Methods. A total of 36 patients with CKD were enrolled in the study. Group A contained patients with CKD stage II; group B with CKD stage III; and group C with CKD stage IV. The control group D consisted of 30 healthy subjects. In the serum, we determined the following: intact parathormon, total calcium, creatinine; in the red blood cells: free cytosolic calcium concentration (Ca_i²⁺), activity of Ca²⁺–Mg²⁺-transporting ATPase (PMCA), basal PMCA (bPMCA), calmodulin (CALM), CANP, CAST.

Results. In all groups, Ca_i²⁺ concentrations were significantly higher, whereas PMCA and bPMCA activity were lower than in the controls. CANP concentrations in group A were elevated compared to the controls, whereas in groups B and C they were significantly lower. In group C, the mean CAST activity reached the highest values. CALM concentrations were decreased versus controls in all groups of patients.

Conclusions. The intracellular Ca_i²⁺ homeostasis is disturbed in children with CKD and aggravates the deterioration of renal function as well. The reasons for the progressing increase of erythrocyte calcium concentration are multifactorial. Undoubtedly, the decreased PMCA activity, the calmodulin deficiency and the dysregulated CANP–CAST system are responsible for that phenomenon. The impact of many other biological modulators, creating a network defending the cell against the calcium accumulation, cannot be excluded.

Methods. A cross-sectional study was performed in 1197 patients with type 2 diabetes mellitus. The estimated glomerular filtration rate (eGFR) was calculated using the formula recommended by the Japanese Society of Nephrology.

Results. The groups with normoalbuminuria, microalbuminuria, macroalbuminuria and renal failure consisted of 696 (58%), 229 (19%), 196 (16%) and 76 (6%) subjects, respectively. The frequencies of all diabetic micro- and macroangiopathies increased with progression of diabetic nephropathy stage. However, in the groups with chronic kidney disease (CKD) stage 3+4 (60 > eGFR ≥ 15 mL/min/1.73 m²), the frequencies of diabetic neuropathy and macroangiopathies were not different among the groups staged by urinary albumin excretion. In the normoalbuminuria group, 223 (32%) cases showed CKD stage 3+4. Diabetic neuropathy and macroangiopathies were significantly more frequent in the groups presenting with normoalbuminuria with CKD stage 3+4 than in those with CKD stage 1+2 (eGFR ≥ 60 mL/min/1.73 m²). The patients' age, duration of diabetes mellitus and frequency of hypertension were significantly higher in the groups presenting with normoalbuminuria with CKD stage 3+4. After adjustment by age, grade of albuminuria or both, CKD stage 3+4 was an independent risk factor for some diabetic complications.

Conclusions. The combination of urinary albumin excretion and eGFR is useful for earlier detection of kidney and vascular damage in patients with diabetes mellitus. Evaluation of eGFR should be performed for all diabetic patients even if they show normoalbuminuria.

Methods. We enrolled patients undergoing creation of primary RCAVF for haemodialysis based on the pre-operative ultrasound vascular mapping discussed in a multidisciplinary approach. Intra-operative blood flow measurement was systematically performed once the anastomosis had been completed using a transit-time ultrasonic flowmeter. During the follow-up, blood flow was estimated by colour flow ultrasound at various intervals. Any events related to the RCAVF were recorded.

Results. Autogenous RCAVFs (n = 58) in 58 patients were constructed and followed up for an average of 30 days. Thrombosis and non-maturation occurred in eight (14%) and four (7%) patients, respectively. The intra-operative blood flow in functioning RCAVFs was significantly higher compared to non-functioning RCAVFs (230 vs 98 mL/min; P = 0.007), as well as 1 week (753 vs 228 mL/min; P = 0.0008) and 4 weeks (915 vs 245 mL/min, P < 0.0001) later. Blood flow volume measurements with a cut-off value of 120 mL/min had a sensitivity of 67%, specificity of 75% and positive predictive value of 91%.

Conclusions. Blood flow <120 mL has a good predictive value for early failure in RCAVF. During the procedure, this cut-off value may be used to select appropriately which RCAVF should be investigated in the operation theatre in order to correct in real time any abnormality.

Methods. All transplant units were invited to participate; four agreed to do so, contributing 36 patients awaiting liver transplantation. Blood was collected from these 36 and divided into aliquots then sent to the four participating centres. Every centre measured creatinine and bilirubin for every patient. The results were analysed for the degree of agreement between centres for creatinine and MELD scores using the Bland–Altman method and Wilcoxon rank test.

Results. The mean creatinine value varied from 101 µmol/l in centre C to 110 µmol/l for the same sample in centre A, with significant differences between the four centres (P < 0.05, Wilcoxon signed-rank test). The MELD scores were significantly different between centre C and all other centres (P < 0.05).

Conclusion. This study demonstrates lack of agreement in measurement of serum creatinine and MELD scoring between four UK transplant centres. A difference in two MELD points can have a significant impact on patient outcome, and these factors will have to be addressed if a UK-wide transplant list is to be initiated.

Methods: To determine the background levels of genetic damage and its specific levels of oxidative damage, a large population of 253 CRF patients (77 in dialysis) was analysed using the comet assay. The percentage of DNA in the tail was used as a measure of basal genetic damage. In addition, the use of endo III and FPG enzymes allowed us to determine the levels of specific oxidative damage in DNA bases.

Results: This is the first study that uses endo III and FPG enzymes to measure oxidative damage in CRF patients. Overall genetic damage, as well as specific oxidative damage, was higher in dialysis patients than in the CRF patients with different stages of uraemic state; genetic damage increased when serum creatinine levels increased. Genomic damage in dialysis patients decreased in those patients submitted to dialysis for a long time.

Conclusions: Genetic damage increases when renal function decreases, being maximum in haemodialysis patients. Although part of the observed damage can be attributed to the uraemic state itself, other individual genetic factors can influence a state of genomic instability responsible for the observed genomic damage.

Methods. SCID mice were divided into three groups: normal, AN + hamster IgG (ADR+IgG group) and AN + anti-CD154 antibody (MR1) (ADR+MR1 group). AN was induced by tail vein injection of 5.2 mg/kg of adriamycin (ADR). Hamster IgG (control Ab) or MR1 was administered intraperitoneally on days 5, 7, 9 and 11 after ADR injection. Histological and functional data were collected 4 weeks after ADR injection. In vitro experiments tested the effect of soluble and cell-bound CD154 co-cultured with CD40-expressing cells [macrophages, mesangial cells and renal tubular epithelial cells (RTEC)].

Results. All experimental animals developed nephropathy. Compared to the ADR+IgG group, ADR+MR1 animals had significantly less histological injury (glomerulosclerosis and tubular atrophy) and functional injury (creatinine clearance). Kidneys of ADR+MR1 animals had significantly less macrophage infiltration than those of ADR+IgG animals. Interestingly, expression of CD40 and CD41 (a platelet-specific marker) was significantly less in ADR+MR1 animals compared to ADR+IgG animals. In vitro, CD154 blockade significantly attenuated upregulation of CCL2 gene expression by RTEC stimulated by activated macrophage-conditioned medium. In contrast, platelet-induced upregulation of macrophage and mesangial cell proinflammatory cytokine gene expression were not CD154-dependent.

Conclusion. CD40–CD154 blockade has a significant innate renoprotective effect in ADR nephrosis. This is potentially due to inhibition of macrophage-derived soluble CD154.

Patients and methods. Mean age at the start of the study was 8 years and 3 months, and all children had been receiving rhGH treatment for >12 months before enrolment. Mean follow-up time on D-OL-HDF was 20.5 ± 8 months (range, 11–39 months). Renal residual function was either <3 mL/min/1.73 m² or anuric. Vascular access was a fistula (13/15) or a central venous catheter (2/15). Dialysis was delivered daily, six days a week in 3 hourly sessions (18 h/week), in a predilution OL-HDF mode, allowing a high convective volume (18 to 27 L/m² body surface area per session), Kt/V_urea on line measured at least 1.4 per session.

Results. Mean growth velocity increased from 3.8 ± 1.1 cm/year at inclusion to 14.3 ± 3.8 cm/year during the first year of D-OL-HDF, resulting in a change in height standard deviation score (SDS) over the follow-up period from –1.5 ± 0.3 SDS to +0.2 ± 1.1 SDS. Increase in body mass was also noted without impaired control of blood pressure. Time-average deviation for urea (TAD_urea) was low at 2.5 ± 0.4 as was TAD_bicarbonate due to the normal pre and post dialysis bicarbonate levels, respectively, 23.6 ± 0.5 mmol/L and 26.6 ± 0.5 mmol/L. The absence of any dietary restrictions permitted a mean protein diet intake (PDI) of 2.5 ± 0.2 g/kg/day (PDI measured from a 3-day diet survey), contrasting with a mean normalized protein nitrogen appearance (nPNA) of 1.53 ± 0.12 g/kg/day (nPNA calculated from urea dialytic kinetic). A low C-reactive protein was noted in 13/15 children, and mean β₂ microglobulin was low, 15.3 ± 0.3.3 mg/L.

Conclusions. Daily OL-HDF promotes catch-up growth in children despite on chronic dialysis. This catch-up growth if continued, should allow the children to reach their mid-parental target height in the future. It could be speculated that the improved response to rhGH is the result of several combined factors conducting to less malnutrition and to less cachexia.

Methods. The study used a retrospective cohort of adult patients in a hypertension registry in an inner-city health care delivery system in Denver, Colorado. The primary outcome was development of incident CKD, and the secondary outcome was rate of change of estimated glomerular filtration rate (eGFR) over time.

Results. After a mean follow-up of 45 months, 429 (4.1%) of 10 420 patients with hypertension developed CKD. In multivariate models, factors that independently predicted incident CKD were baseline age [odds ratio (OR) 1.13 per 10 years, 95% confidence interval (CI), 1.03–1.24], baseline eGFR (OR 0.69 per 10 units, 95% CI 0.65–0.73), diabetes (OR 3.66, 95% CI 2.97–4.51) and vascular disease (OR 1.67, 95% CI 1.32–2.10). We found no independent association between age, gender or race/ethnicity and eGFR slope. In patients who did not have diabetes or vascular disease, eGFR declined at 1.5 mL/min/1.73 m² per year. Diabetes at baseline was associated with an additional decline of 1.38 mL/min/1.73 m².

Conclusions. Diabetes was the strongest predictor of both incident CKD as well as eGFR slope. Rates of incident CKD or in decline of kidney function did not differ by race or ethnicity in this cohort.

Methods. Cell migration was determined by a modified Boyden chamber assay. The intracellular signalling pathway was examined by western blotting. AT1 receptor expression was knocked down by small interfering RNAs. The intracellular reactive oxygen species (ROS) was measured by using a fluorescent probe. The O₂^·– scavenging activities were studied by the electron paramagnetic resonance-spin trapping method.

Results. PDGF-induced cell migration was inhibited by olmesartan in AT1 receptor knockdown RMCs. Olmesartan attenuated big mitogen-activated protein (MAP) kinase 1 (BMK1) and Src activation by PDGF in AT1 receptor knockdown RMCs. PDGF-induced BMK1 activation was suppressed by the Src family tyrosine kinase inhibitors, indicating that Src exists upstream of BMK1. The NADPH oxidase inhibitors inhibited not only PDGF-induced BMK1 and Src activation but also RMC migration. The elevation in ROS generation induced by PDGF was decreased by olmesartan. Olmesartan displayed neither directly ROS scavenging activity nor the inhibition of ROS-mediated intracellular signalling in RMCs.

Conclusions. Olmesartan attenuates ROS generation by PDGF, leading to the subsequent inhibition of Src/ BMK1/migration in an AT1 receptor-independent manner in RMCs.

Methods. The Study on Evaluation of Candesartan Cilexetil after Renal Transplantation (SECRET) was an international multicentre, double-blind, randomized investigation of the angiotensin II type 1 receptor blocker (ARB) candesartan cilexetil versus placebo in renal allograft recipients originally designed to study 700 patients for 3 years. The candesartan dose was escalated from 4 to 16 mg daily, followed by addition of co-medication, if needed, with the aim of achieving a diastolic blood pressure (BP) <85 mmHg. The primary efficacy variable was a composite of all-cause mortality, cardiovascular morbidity and graft failure.

Results. SECRET was stopped prematurely as the primary event rate was much lower than expected. At that point, 502 patients were enrolled; 255 received candesartan and 247 placebo. Thirteen primary events had occurred in each group. Control of both systolic and diastolic BP was better in the candesartan group. Urinary protein excretion and protein/creatinine ratio decreased on candesartan but increased on placebo. Serum creatinine and potassium were increased in candesartan patients, but these changes were generally small.

Conclusions. SECRET provides insights into the design and conduct of studies in this area and evidence for the utility of candesartan, which showed good safety and tolerability, improved BP control and decreased proteinuria in renal transplant recipients.

Methods. An endotoxaemic rat model of ARF was induced by renal artery occlusion plus subcutaneous injections of Escherichia coli in 4-week-old Wistar rats. A subset of rats was given intraperitoneal injection of the adeno-β₂-AR gene.

Results. Sepsis produced a depression in glomerular filtration rate and in the renal β₂-AR signalling system, which were both reversed by delivery of the β₂-AR gene. While delivery of the adeno-β₂-AR gene had no effect on recovery of cytokines and C-reactive protein in the systemic circulation, it did significantly depress (P < 0.01) the expression of the renal cannabinoid-1 (CB-1) receptor, CD14, toll-like receptor 4 (TLR4) and tumour necrosis factor (TNF)- protein. Gene delivery also increased nitric oxide (NO) and decreased angiotensin II (Ang II). Finally, transfer of the β₂-AR gene also improved the survival of the rats exposed to sepsis-induced ARF.

Conclusions. A renal-specific over-expression of β₂-AR, resulting from gene delivery, appeared to modulate renal dysfunction and inflammation following sepsis by altering cAMP–PKA, CB-1 and CD14–TLR4–TNF- pathways. In addition, gene delivery and activation of β₂-AR produced modulation of systemic NO and Ang II, which further protected against renal dysfunction. Administration of the Adeno-β₂-AR gene has potential as a therapeutic agent against ARF following the onset of sepsis.

Methods. Eighty-three patients without diabetes were randomly assigned to either the pioglitazone group or the control group. Carotid intima–media thickness (IMT), serum adiponectin level and lipid profile were assessed before transplantation and at 12 months after transplantation. Insulin secretory function and insulin resistance were evaluated by the oral glucose tolerance test.

Results. The pioglitazone group showed a significant reduction in the mean and maximum carotid IMT compared with the control group after 12 months (mean carotid IMT, 0.05 ± 0.04 vs –0.03 ± 0.07 mm, P < 0.001; maximum carotid IMT, 0.08 ± 0.05 vs –0.05 ± 0.09 mm, P < 0.001). Pioglitazone increased the adiponectin level, and the change in adiponectin was negatively correlated with carotid IMT changes. Pioglitazone treatment increased the insulin sensitivity index compared with the control group (–0.8 ± 3.1x10^–2 vs +1.1 ± 3.7x10^–2, P = 0.036).

Conclusions. These results suggest that pioglitazone treatment reduces the progression of carotid IMT and improves insulin resistance in renal allograft recipients without a history of diabetes.

Trial Registration. Clinicaltrials.gov Identifier: NCT00598013

Methods. We audited pre-midweek session calcium and phosphate levels in 5366 adult patients, 4515 treated by haemodialysis and 851 by on-line haemodiafiltration.

Results. The cohorts were similar for age, sex and dialysis vintage. Serum phosphate was lower in the haemodiafiltration cohort (1.42 ± 0.61 mmol/l) compared to the haemodialysis cohort (1.53 ± 0.53 mmol/l; P < 0.001), as was the calcium–phosphate product (3.31 ± 1.53 vs 3.5 ± 1.33 mmol²/l², respectively; P < 0.001) despite a shorter treatment session time (3.68 ± 0.44 vs 3.92 ± 0.49 h; P < 0.001). Parathyroid hormone levels were similar.

Conclusions. The results of this audit suggest that haemodiafiltration offers improved phosphate control compared to standard intermittent haemodialysis.

Methods. All the files kept in the Renal Unit were reviewed for the main clinical presentation, a definitive pathological diagnosis (if obtained), age, race and gender of the patients. No consultations from other disciplines were included.

Results. One thousand two hundred and sixteen patients were included in the study. The main clinical presentations were as follows: chronic renal failure (CRF), 461 (37.9%); nephrotic syndrome, 203 (16.7%); hypertension, 161 (13.2%); and abnormal urinary findings, 128 (10.5%). The nephrotic syndrome was the most common indication for renal biopsy, and histological investigation revealed focal segmental glomerulosclerosis in 46 (3.8%) patients, minimal change in 23 (1.9%), membranoproliferative disease in 36 (3.0%) and membranous glomerular disease (MN) in 28 (2.3%). In CRF, hypertension was suspected in 236/461 (51.2%) cases but was proven histologically in only 13 (2.8%) patients.

Conclusions. Socio-political factors impacting on access to healthcare most likely had an influence on the referral pattern of patients during this period. The largest group of patients were referred to our institution late in their disease with CRF, often requiring renal replacement therapy, and a definitive diagnosis was seldom possible at that stage. With the limited availability of dialysis facilities, the need for early detection and preventative measures with regard to renal disease in this community is evident.

Methods. Thirty-nine ESRD patients on regular dialysis underwent elective coronary angiography. Coronary artery stenosis >75% was defined as significant. TFC for the three main coronary vessels was calculated. Higher TFC values reflected slower flow.

Results. In 19 patients (49%), significant epicardial coronary artery disease was found. Distribution of the TFC for the three main coronary arteries reflected prevalence for higher TFC values. Mean corrected TFC for the left anterior descending artery (LAD) was 34.7 ± 16, for the circumflex artery (Cx) 41.5 ± 25 and for the right coronary artery (RCA) 30.9 ± 18 frames.

For the three main coronary vessels, there were no statistically significant differences between the mean TFC values according to the presence or absence of the severe coronary artery stenoses on angiography (LAD: 30.2 ± 12 vs 36.3 ± 18; Cx: 41.5 ± 20 vs 41.5 ± 27; RCA: 34.9 ± 16 vs 30.0 ± 19, respectively).

Conclusions. Our results demonstrate for the first time the reduction in blood flow velocity, assessed with TFC method, in the coronary arteries of ESRD patients. This phenomenon was observed regardless of the presence of the significant epicardial coronary artery stenosis. Therefore, TFC cannot be applied as a marker of significant coronary artery stenosis in ESRD population.

Methods. Incident patients on chronic RRT in the period 2001–2004 were identified in NRDT and in the National Patient Registry, which contains information on hospital admissions and treatments. In the National Patient Registry, identification of patients was as follows: patients receiving the procedure of dialysis during a minimum of 90 days and for a minimum of 12 times or the procedure of renal transplantation. Only patients with at least 2 years of dialysis-free interval before and never being transplanted were included. The completeness of NRDT was calculated as the percentage of new patients on chronic RRT registered in the National Patient Registry also found in NRDT. Validity of data in NRDT was assessed by information from medical records and analysed using kappa statistics.

Results. Completeness of NRDT: Of 3020 patients registered in the National Patient Registry as incident chronic RRT patients, 97.2% were found in NRDT but 22.5% with another year of entry. There were no differences in completeness between hospitals or regions. Validity of NRDT: Validity of common renal diagnoses and RRT modality was high: diabetic nephropathy (kappa = 0.98), adult polycystic kidney disease (kappa = 0.95), chronic glomerulonephritis (kappa = 0.78) and RRT modality (kappa = 0.94). The diagnosis CKD of unknown aetiology and type of diabetes were less valid (kappa = 0.62, 0.60 and 0.73, respectively). The date of RRT start had also high validity.

Conclusions. Completeness of incident patient registration in NRDT was highly acceptable. Validity of incident patient data was also good, except for type of diabetes.

Methods. A 3.25-year-old girl presenting with childhood-onset heavy proteinuria, bilateral myosis and nystagmus was detected on mutations of LAMB2 gene by PCR direct sequencing.

Results. Two novel mutations were identified, C757fsX767 and P1413fsX1451, which predicted truncated proteins and were confirmed in the paternal and maternal origins, respectively.

Conclusions. This is the first Chinese case of Pierson syndrome diagnosed by clinical manifestations and LAMB2 gene mutations. The phenotype may be different in different ethics.

Methods. Peritonitis was induced in CD1 mice by intraperitoneal injection of Escherichia coli. TNF and IL-6 levels were determined in peritoneal fluid by enzyme-linked immunosorbent assay. Adenosine-metabolizing enzymes and the A₁R mRNA or protein levels were analyzed by quantitative PCR or by Western blot analysis, respectively.

Results. We found that CD39 and CD73 were up-regulated in response to bacterial stimuli (6-fold the basal levels), while AK and ADA mRNA levels were down-regulated. Cytokine production and leukocyte recruitment were enhanced (2.5-fold) by treatment with an A₁R agonist (2-chloro-N⁶-cyclopentyladenosine, 0.1 mg/kg) and reduced (2.5–3-fold) by the A₁R antagonist (8-cyclopentyl-1, 3-dipropylxanthine, 1 mg/kg). In contrast to lipopolysaccharide, IL-1, TNF and IFN, only low IL-6 levels (0.01 ng/ml), in the presence of its soluble IL-6R (sIL-6R), were found to promote A₁R expression on mesothelial cells. In mice, administration of neutralizing antibody to IL-6R or soluble gp130-Fc (sgp130-Fc) blocked peritoneal A₁R up-regulation following inoculation.

Conclusion. Bacterial products induce the production of adenosine by up-regulation of CD39 and CD73. Low IL-6–sIL-6R up-regulates the A₁R to promote efficient inflammatory response against invading microorganisms.

Methods. The study was a prospective non-randomized study of consecutive cases of secondary CNS. Patients with idiopathic CNS were excluded.

Results. Twenty-four of 78 (30.8%) CNS cases were of secondary aetiology. Overall mean ages at onset of secondary CNS aetiology and CNS onset were 8.97 ± 3.59 (1–15.3) and 9.95 ± 3.15 (5–15.3) years, respectively. Male (14)/female (10) ratio was 1.4. Secondary causes comprised systemic lupus erythematosus (SLE, 37.5%), sickle cell anaemia (SCA, 16.7%), hepatitis B virus (HBV, 16.7%) infection, Churg–Strauss syndrome (12.6%), SLE/human immunodeficiency virus infection (4.2%), rhabdomyosarcoma (4.2%), bee stings (4.2%) and Addison's disease (4.2%). The overall cumulative complete remission (CR) rate was 88.0%. Remission was sustained in 11 of 16 (68.8%) CR patients, while one patient (6.25%) relapsed; the remaining four patients (24.95%) were yet to attain sustained remission. Median relapse-free period was 10.5 (0.75–25) months. Cumulative renal survival was 75.2% at 3 years. Three patients were lost to follow-up, while two died. Overall cumulative patient survival probability at 36 months was 90.8%. All patients were followed for a median period of 12.5 (0.11–36.0) months.

Conclusion. Overall outcome of CNS has improved significantly compared to the 1960s and 1970s when the poor outcome of QMN was the predominant glomerular lesion in Nigeria. While quartan malaria-associated nephrotic syndrome has become a rare clinical entity, SLE, SCA and HBV infection have become the major secondary aetiologies of CNS in Nigeria.

Methods. Acute pyelonephritis was diagnosed in 104 children (63 males) aged 2 months to 12 years by urine culture and 99Tc-DMSA renal scan. A follow-up isotope scan was performed 4–6 months later to identify new renal scar formation. Vesicoureteral reflux (VUR) was examined by micturating cystourethrogram. Controls comprised 300 healthy children with no evidence of renal disease. Three single-nucleotide polymorphisms (SNPs) in the TGFβ-1 (–800 A/G, –509 C/T and 869 C/T) and four SNPs in the VEGF gene (–2578 C/A, –1154 G/A, –460 T/C and +405 G/C) were genotyped in all subjects.

Results. Forty-six of the 104 patients developed renal parenchymal scarring (44.2%). VUR was found in 35.6%. The –509 T allele in the TGFβ-1 promoter was significantly more common in cases with renal scarring (51%) than in non-scarring patients (22.4%) and controls (23.6%) (both P < 0.0001). At the haplotype level, the GTC combination at –800/–509/+869 was strongly associated with renal scarring (P = 0.0002). VEGF–460 CC was more common in UTI cases with renal scarring than in non-scarring patients and controls (P = 0.03 and 0.001, respectively). Multiple logistic regression testing identified the presence of VUR (odds ratio 12.4, CI 3.8–40; P < 0.001) and the TGFβ-1 –509 T allele (OR 6.1, CI 2.4–15.5; P < 0.001) as independent risk factors for renal scarring after UTI. In contrast, age, gender and the type of underlying organism were not predictive of renal scarring.

Conclusions. Activating variants in the TGFβ-1 and VEGF gene promoters are associated with post-UTI renal scar formation in children. The TGFβ-1 509T allele predicts renal scarring independent of VUR.

Methods. This is a retrospective cohort study involving 301 patients without pre-transplant DM. Measurements included a pre- and post-transplant oral glucose tolerance test (OGTT) as well as glomerular filtration rate (GFR), parathyroid hormone (PTH), phosphate, calcium and urea measured 10 weeks post-transplant. The risk of PHYG at 10 weeks post-transplant was analysed using multiple logistic regression.

Results. Ninety-three patients (31%) had PHYG (two IFG, 52 IGT, 39 DM). Variables associated with PHYG included pre-transplant 2-h glycaemia [OR 1.26, 95% CI (1.09, 1.46)] and post-transplant urea levels [OR 1.14, 95% CI (1.02, 1.27)]. Older age, non-Caucasian ethnicity, previous transplants, ≥3 HLA class 1 mismatches and high prednisolone doses were likewise associated with an increased PHYG risk (all P < 0.05).

Conclusions. Pre-transplant glycaemia and high post-transplant levels of urea were associated with a greater risk of PHYG. This seemed to be independent of GFR, PTH, phosphate, calcium and traditional risk factors such as age and glucocorticoid load.

Methods. Carotid-femoral pulse wave velocity (PWV; an index of arterial stiffness) was measured in 264 subjects with chronic kidney disease (CKD) stages 3–5 from three nephrology clinics (‘lower GFR group’). PWV was also measured in 149 subjects without previously recognized CKD (‘higher GFR group’) including n = 26 with eGFR between 30 and 60 ml/min/1.73 m² and n = 123 with eGFR between 60 and 100 ml/min/1.73 m². The association between PWV and eGFR was investigated using linear regression.

Results. The 413 subjects had a mean age of 61.9 years, were 51% male, 28% diabetic and 79% hypertensive. In age-adjusted analyses within the ‘lower GFR group’, ‘higher GFR group’ and combined group, PWV correlated with higher systolic blood pressure (SBP), pulse pressure (PP), diabetes mellitus, body mass index (BMI) and resting heart rate (all P < 0.0008). In addition, PWV correlated inversely with eGFR in the ‘higher GFR group’ (P = 0.03) and combined group (P < 0.0001). In multivariable regression analyses of the combined group (n = 413), PWV was independently predicted by eGFR (P < 0.05). However, eGFR explained at most 4% of the variability in PWV in age-adjusted analyses (compared with 13–15% explained by SBP, PP or diabetes) and <1% of PWV variability in models adjusting for age, SBP, diabetes, heart rate and BMI (P < 0.0001).

Conclusion. Although eGFR may independently predict PWV, the contribution of GFR per se does not appear to be clinically meaningful when compared with traditional cardiovascular risk factors.

Methods. Using a genetically defined mouse model of XLAS, we generated two groups of Alport female (Col4a5^+/–) carriers that differed only in the X-controlling element (Xce) allele regulating X-inactivation. We followed the groups as far as 6 months of age comparing survival and surrogate outcome measures of urine protein and plasma urea nitrogen.

Results. Preferential inactivation of the mutant Col4a5 gene improved survival and surrogate outcome measures of urine protein and plasma urea nitrogen. In studies of surviving mice, we found that X-inactivation in kidney, measured by allele-specific mRNA expression assays, correlated with surrogate outcomes.

Conclusions. Our findings establish X-inactivation as a major modifier of the carrier phenotype in X-linked Alport syndrome. Thus, X-inactivation patterns may offer prognostic information and point to possible treatment strategies for symptomatic carriers.

Methods. Serum levels of the biologically active hepcidin-25 and its isoforms were determined in CKD and dialysis patients by a mass spectrometry-based assay.

Results. In 83 patients with CKD not requiring dialysis, serum hepcidin-25 levels were not significantly increased (5.1 nM versus 4.2 nM, P = 0.30) and positively correlated with ferritin (r = 0.74, P < 0.01). Multiple regression analysis showed ferritin to be the only significant predictor of hepcidin-25 levels. Serum hepcidin-25 levels were not dependent on eGFR. In contrast, hepcidin-20 and total hepcidin levels showed an independent significant inverse correlation with eGFR. In 48 haemodialysis patients, median hepcidin-25 levels were significantly higher than in CKD patients (9.4 nM versus 5.1 nM, P < 0.001) and again strongly correlated with ferritin (r = 0.79, P < 0.001).

Conclusions. eGFR is not a major determinant of serum hepcidin-25 levels. In contrast, the hepcidin isoforms hepcidin-20 and hepcidin-22 accumulate in patients with renal impairment.

Methods. Urea kinetic modelling, continuous sampling of spent dialysate and ionic dialysance were determined in 18 stable dialysis patients during 126 dialysis sessions. Mean blood urea levels were estimated as follows: mean urea level = spent dialysate – urea mass/(dialysance * T). Blood urea levels before and after dialysis were calculated based on the same determinations and extended formulae.

Results. Estimated mean urea level was significantly correlated with measured mean blood urea level (R² = 0.957; P < 0.0001), and Bland and Altman analysis showed significant agreement between estimated and measured levels. Estimated and measured blood urea levels were also correlated before and after dialysis (R² = 0.972 , P < 0.0001 and R² = 0.903 , P < 0.0001, respectively), with good agreement for both blood urea before and after dialysis and their respective estimates.

Conclusions. Blood urea levels may be reliably estimated from the total mass of urea removed in the dialysate and the dialysance measured during dialysis. Coupling both measurements allows a precise monitoring of dialysis efficacy and a specific evaluation of the patient’s urea metabolism status. Technical dysfunctions and patient variations may be easily identified using this approach without blood sampling.

Methods. Pre-diabetes and an insulin sensitivity index were estimated by an oral glucose tolerance test in 66 consecutive uraemic patients, without diabetes, being on the waiting list for the first renal transplantation. Mean age was 43 ± 13 years. Duration of ESRD was 32 ± 27 months. A control group consisted of 14 healthy subjects.

Arterial stiffness was measured by aorta pulse wave velocity (PWV) and aorta augmentation index (AIX). Endothelial function was evaluated by flow-mediated vasodilatation (FMD) and plasma concentrations of von Willebrand factor antigen (vWF). Mean arterial blood pressure (MAP) was measured in supine resting position.

Results. Twenty-seven uraemic patients (41%) had pre-diabetes (IFG+IGT), and 39 had normal glucose tolerance. The uraemic patients were more insulin resistant with lower insulin sensitivity index compared to healthy controls (6.1 ± 3 vs. 15 ± 7, P < 0.0001) but with no difference between patients with and without pre-diabetes. HbA1c and fasting plasma glucose was comparable in uraemic patients with and without pre-diabetes.

PWV was higher in pre-diabetic compared to normoglycaemic uraemic patients (9.1 ± 3 vs. 7.3 ± 2 m/s, P = 0.03) and healthy controls (9.1 ± 3 vs. 6.7 ± 1, P = 0.01), while AIX did not differ (24.9 ± 13 vs. 23.2 ± 12 vs. 17 ± 16, P = NS). Presence of pre-diabetes was positively associated to PWV in a univariate analysis. Multivariable analysis revealed age and MAP as independent predictors of PWV in uraemic patients. FMD and vWF were impaired in uraemic patients compared to healthy controls (3 ± 4 vs. 7 ± 3, P = 0.007 and 1.8 ± 0.7 vs. 0.96 ± 0.3 kIU/L, P = 0.0002, respectively) but with no difference between the two groups of uraemic patients.

In conclusion, a high prevalence of pre-diabetes, impaired insulin resistance, increased arterial stiffness of aorta as well as impaired augmentation index and vasodilatation was demonstrated in uraemic patients prior to kidney transplantation. Increased arterial stiffness of aorta and augmentation index were independently associated with age and blood pressure.

Methods. The survey was developed in Lotus Notes with a secure browser-based form. The form was open to 602 Fresenius Medical Care clinics located in Europe, Middle East, Africa and Latin America.

Results. As of 3 September 2009, 306 cases have been reported by 85 clinics located in Argentina, Chile, Brazil, UK and Spain. The mean age was 52.7 ± 17.7 years. The majority of cases (70.6%) were from 20–44- and 45–64-year-old subgroups. Moreover, 35.3% had no associated comorbidity, 20.3% had two and 4.6% three comorbidities, with heart disease being the most frequent. Fever was the most common symptom, present in 94.4% of the cases, followed by cough (78.8%) and muscle and joint pain (69.3%). Eighty-seven percent were treated with antiviral agents, the majority with oseltamivir. One hundred and three patients (34%) were admitted to hospital because of influenza. Pneumonia was reported for 69 cases, out of which 52 patients belonged to a high-risk group. Mortality rate of all the patients (confirmed, probable and suspected cases) was around 5%.

Conclusion. End-stage renal disease patients should be included in first ranks of the priority list for the influenza A(H1N1)v vaccine, as already advocated by some healthcare authorities.

Methods. Patients who entered RRT because of type 2 diabetes mellitus in 1995–99 (n = 314) and 2000–05 (n = 583) were identified within the Finnish Registry for Kidney Diseases. The two cohorts were followed up from start of RRT until death or end of follow-up on 31 December 2006. Survival probabilities and probabilities of receiving a kidney transplant were calculated using Kaplan–Meier curves. Multivariate modelling was performed using Cox regression.

Results. Patients who entered RRT in 2000–05 had lower risk of dying than those who entered in 1995–99; hazard ratio (HR) was 0.76 (95% CI 0.65–0.89) and 0.74 (95% CI 0.63–0.87) with adjustment for age and gender. The decreased risk of death was most obvious in age groups 55–64 (HR 0.67, 95% CI 0.49–0.92) and 65–74 years (HR 0.69, 95% CI 0.56–0.87). Adjustment for albumin in addition to age and gender only slightly weakened the effect of study periods (HR 0.83, 95% CI 0.69–1.01). The patients in 2000–05 were more obese, had lower total and LDL cholesterol and higher HDL cholesterol and albumin concentration in serum than patients in 1995–99. Patients' probability to receive a kidney transplant was low in both groups.

Conclusions. Survival of type 2 diabetes patients on RRT improved during the time period 1995–2005 in Finland while the probability of receiving a kidney transplant remained low and unchanged.

Methods. Data from 2712 patients in the Fabry Registry were analysed to identify clinical characteristics of patients who received renal replacement therapy (RRT) during the natural history period (i.e. prior to any enzyme replacement therapy).

Results. A total of 213 patients [186 of 1359 males (14%) and 27 of 1353 females (2%)] received RRT at a median age of 38 years in both males and females. Males who received RRT were diagnosed at a median age of 35 years, compared to 23 years for non-RRT males. Sixty-one males and 10 females were not diagnosed with Fabry disease until after they had received RRT. Compared to other Fabry Registry patients, a higher percentage of RRT patients also experienced either a serious cardiovascular event or a stroke. Ninety-two of 186 males who had RRT (50%) experienced a cardiac event or stroke, compared to 230 of 1173 non-RRT males (20%). Ten of 27 RRT females (37%) had experienced a cardiac event or stroke, compared to 226 of 1326 non-RRT females (17%). Patients who had RRT experienced cardiovascular events and strokes at earlier ages than did patients who had not received RRT, and most received RRT before having a cardiac event or stroke.

Conclusions. While all Fabry patients are at risk of cardiovascular events and strokes, patients with Fabry nephropathy who develop kidney failure appear to have concurrent involvement of other major organ systems. It is important that Fabry patients are diagnosed early and that their renal function is monitored carefully.

Methods. As renal phenotype can be influenced by genetic background, we generated congenic C57BL/6 and FVB/N Ctns^–/– mice and assayed renal lesions and function by histological and biochemical studies.

Results. C57BL/6 Ctns^–/– mice showed significantly higher renal cystine levels than the FVB/N strain. Moreover, C57BL/6 mice presented with pronounced histological lesions of the proximal tubules as well as a tubulopathy and progressively developed chronic renal failure. In contrast, renal dysfunction was not observed in the FVB/N strain.

Conclusions. Thus, the C57BL/6 strain represents the first Ctns^–/– mouse model to show clear renal defects. In addition to highlighting the influence of genetic background on phenotype, the C57BL/6 Ctns^–/– mice represent a useful model for further understanding cystinosin function in the kidney and, specifically, in the proximal tubules.

Patients. Thirty-seven children (65% male) with a median age of 7.6 (0.4–17.9) years were identified with a median systolic blood pressure (SBP) of 140 (105–300) mm Hg prior to surgery. Bilateral renal artery stenosis and intra-renal disease were present in 19 (51%) patients, mid-aortic syndrome in 15 (40%), involvement of visceral arteries in eight out of 35 (23%) and coexisting cerebral disease in eight out of 30 (26%) investigated patients.

Results. Surgical procedures (n = 53) included (i) nephrectomy (18, of which two unplanned and two secondary due to technical failure), (ii) renovascular surgery on the renal arteries (28, of which 18 had autologous surgery and 10 synthetic grafts inserted for revascularisation) and (iii) aortic reconstruction with (6) and without (1) a synthetic graft. Post-operative complications were haemorrhage (5), septicaemia (5) and chylous ascites (1). There were no perioperative deaths; two children died during follow-up. The SBP post-surgery improved to a median value of 116 (range 90–160) mm Hg. Twelve months after surgery, 16 (43%) children had normal blood pressure without treatment, 15 (41%) normal or improved on one to four antihypertensive drugs and four (11%) unchanged; no data were available for two (5%) children.

Conclusion. Surgery effectively treated the hypertension of 90% of our children, when performed in conjunction with medical therapy and interventional radiology. In spite of aggressive surgical treatment, RVH is sometimes a progressive disease.

Methods. An international working group of nephrologists from 11 Fabry centres identified adult Fabry patients, and pathologists scored histologic changes on renal biopsies. A standardized scoring system was developed with a modified Delphi technique assessing 59 Fabry nephropathy cases. Each case was scored independently of clinical information by at least three pathologists with an average final score reported.

Results. We assessed 35 males (mean age 36.4 years) and 24 females (43.9 years) who mostly had clinically mild Fabry nephropathy. The average serum creatinine was 1.3 mg/dl (114.9 µmol/l); estimated glomerular filtration rate was 81.7 ml/min/1.73 m² and urine protein to creatinine ratio was 1.08 g/g (122.0 mg/mmol). Males had greater podocyte vacuolization on light microscopy (mean score) and glycosphingolipid inclusions on semi-thin sections than females. Males also had significantly more proximal tubule, peritubular capillary and vascular intimal inclusions. Arteriolar hyalinosis was similar, but females had significantly more arterial hyalinosis. Chronic kidney disease stage correlated with arterial and glomerular sclerosis scores. Significant changes, including segmental and global sclerosis, and interstitial fibrosis were seen even in patients with stage 1–2 chronic kidney disease with minimal proteinuria.

Conclusions. The development of a standardized scoring system of both disease-specific lesions, i.e. lipid deposition related, and general lesions of progression, i.e. fibrosis and sclerosis, showed a spectrum of histologic appearances even in early clinical stage of Fabry nephropathy. These findings support the role of kidney biopsy in the baseline evaluation of Fabry nephropathy, even with mild clinical disease. The scoring system will be useful for longitudinal assessment of prognosis and responses to therapy for Fabry nephropathy.

Materials and methods. We undertook a retrospective single-centre study in order to assess the rate, risk factors and outcome of HSCT-associated CKD in 123 allogeneic HSCT patients.

Results. Twenty-four months after HSCT, CKD [e.g. glomerular filtration rate (GFR) estimated using the MDRD formula <60 ml/min/1.73 m²] was noted in 49 patients (40%). Age ≥ 45 years, early acute kidney injury and a baseline GFR < 90 ml/min/1.73 m² predicted the occurrence of CKD at 24 months after HSCT. One hundred and six patients (45 with and 61 without CKD at 24 months) were followed up for more than 36 months (range 36–142). Among the 45 patients with CKD at 24 months after HSCT, CKD persisted in 30 (67%), 10 patients (22%) showed a transient improvement in GFR but retained CKD and 10 patients (22%) had a sustained improvement of GFR. Among 61 patients without CKD at 24 months after HSCT, 3 (5%) developed CKD during the follow-up. Our data indicate that HSCT-related CKD probably includes two subsets: a frequent early-onset CKD, a consequence of ARF in older patients with pre-existent renal impairment, and a rare late-onset CKD occurring more than 2 years following HSCT.

Conclusions. Careful monitoring of renal function is mandatory in patients undergoing HSCT, especially old patients with pre-existent renal impairment.

Methods. RCC cell adhesion to matrix was studied via pre-coating a variety of ECM glycoproteins onto plates. Cancer cell apoptosis and cell cycle were evaluated with flow cytometry using annexin V and propidium iodide stains, respectively. Activation of cellular survival signalling was analysed with western blots, and specific molecular inhibitors were correspondingly employed to block signalling. Hypoxia (<1%) was induced via N₂/CO₂ gas flow in a specialized chamber.

Results. While adherence to col(I) enhanced RCC cell proliferation in general, col(I) and fibronectin, but not fibrinogen, could confer specific anti-apoptotic RR to RCC cells. The radioprotective effect of col(I) was maintained during both hypoxia/reoxygenation and normoxia conditions. In contrast to intact col(I), micronized col(I), lacking the natural fibrillar structure, was not radioprotective. The effect of col(I) in RCC cells is mediated via attenuation of apoptosis rather than cell cycle redistribution, involving the PI3 kinase/Akt pathway but not the MAP kinase pathway.

Conclusions. Adherence to col(I) appears to be a relevant environmental cue enhancing RR in RCC cells, Akt dependently. Our results support inhibition of the PI3-kinase/Akt pathway as a radiosensitizing approach.

Methods. Records of 555 (50 Black; 505 non-Black) sequential renal transplant recipients from a single UK centre were analysed.

Results. Outcomes were significantly worse for Black patients: death-censored graft survival (5-year 66% versus 87%, P = 0.001); halving of year one estimated glomerular filtration rate (mean 8.8 versus 10.8 years, P = 0.008); first-year graft loss (12% versus 3.8%, P = 0.02); and death-censored graft survival in patients surviving the first year with functioning grafts (5-year 77% versus 94%, P = 0.02). Death-censored 5-year graft survival was poorer in Black CYP3A5 expressers than in non-Black CYP3A5 expressers (62% versus 93%, P = 0.002). Following multivariate analysis, the Black group demonstrated poorer graft survival as compared to the non-Black group (hazard ratio 0.46, 95% CI 0.25–0.85, P = 0.002). In a subgroup of genotyped transplant recipients, ethnicity (hazard ratio 0.31, 95% CI 0.15–0.64, P = 0.002), and not CYP3A5 expresser status, persists as an independent risk factor for graft survival following multivariate analysis.

Conclusion. In this cohort of patients with socialized medicine, Black recipients had poorer long-term outcomes than individuals from other ethnic groups. This was independent of CYP3A5 expresser status.

Objective. Here, we observed the impact of discontinuation of angiotensin converting enzyme inhibitors (ACEi)/angiotensin receptors blockers (ARB) in patients with advanced kidney disease.

Methods. 52 patients (21 females and 31 males) with advanced CKD (stages 4 and 5), who attended our low clearance clinic (LCC) in preparation for renal replacement therapy (RRT). Mean age was 73.3 ± 1.8 years with an estimated glomerular filtration rate (eGFR) of 16.38 ± 1 ml/min/1.73 m². Baseline urine protein:creatinine ratio (PCR) was 77 ± 20 mg/mmol. 46% suffered from diabetes mellitus. Patients were followed for at least 12 months before and after ACEi/ARB were stopped.

Results. 12 months after discontinuation of ACEi/ARB eGFR increased significantly to 26.6 ± 2.2 ml/min/ 1.73 m² (p = 0.0001). 61.5% of patients had more than a 25% increase in eGFR, whilst 36.5% had an increase exceeding 50%. There was a significant decline in the eGFR slope –0.39 ± 0.07 in the 12 months preceding discontinuation. The negative slope was reversed +0.48 ± 0.1 (p = 0.0001). Mean arterial blood pressure (MAP) increased from 90 ± 1.8 mmHg to 94 ± 1.3 mmHg (p = 0.02), however ≥50% of patients remained within target. Overall proteinuria was not affected (PCR before = 77 ± 20 and after = 121.6 ± 33.6 mg/mmol).

Conclusion. Discontinuation of ACEi/ARB has undoubtedly delayed the onset of RRT in the majority of those studied. This observation may justify a rethink of our approach to the inhibition of the RAAS in patients with advanced CKD who are nearing the start of RRT.

Methods. We reviewed medical records from 240 consecutive paediatric renal transplantations performed in 219 children, aged less than 19 years, in our centre between April 1987 and March 2007. Data from patients who had been transferred into adult units were extracted from the French registries of dialysis and transplantation.

Results. Among the 219 children who underwent renal transplantation during the study period, 16 (7.3%) developed malignancy. The cumulative incidence of cancer was 1.9, 4.0, 6.9 and 10.2% at 1, 5, 10 and 15 years post-transplantation, respectively. The 10-year incidence of post-transplantation lymphoproliferative disorder (PTLD) was 4.5%. Other identified cancers were Hodgkin lymphoma, Burkitt lymphomas, renal papillary carcinoma, thyroid papillary carcinoma, recurrent ovarian seminoma and skin cancer. The mortality rate was 25% (4/16).

Conclusion. Early detection of cancer in transplant recipients is of great importance. Regular screening for persistent Epstein–Barr virus (EBV) DNA viral load in patients at risk for developing PTLD is recommended. The occurrence of skin cancer in transplanted children is extremely rare during childhood, but cases can develop in early adulthood.

Methods. Nineteen European national or regional renal registries with registry data from 1997 to 2006 participated in the study. Incidence and prevalence trends were analysed with Poisson and Joinpoint regression. Cox regression methods were used to examine patient survival.

Results. The total adjusted incidence rate of RRT for ESRD increased from 109.9 per million population (pmp) in 1997 to 119.7 pmp in 2000, i.e. an average annual percentage change (AAPC) of 2.9% (95% CI 2.1–3.8%). Thereafter, the incidence increased at a much lower rate to 125.4 pmp in 2006 [AAPC 0.6% (95% CI 0.3–0.8%)]. This change in the trend of the incidence of RRT was largely due to a stabilization in the incidence rates of RRT for females aged 65–74 years, males aged 75–84 years and patients receiving RRT for ESRD due to hypertension/renal vascular disease. The overall adjusted prevalence in Europe continued to increase linearly at 2.7% per year. Between the periods 1997–2001 and 2002–2006, the risk of death decreased for all treatment modalities, with the most substantial improvement in patients starting peritoneal dialysis [19% (95% CI 15–22%)] and in patients receiving a kidney transplant [17% (95% CI 11–23%)].

Conclusion. This European study shows that the annual rise of the overall incidence rate of RRT for ESRD has diminished and that in several age groups the incidence rates have now stabilized. The survival of dialysis patients and kidney transplant recipients has continued to improve.

Methods. The aim of this retrospective study was to review the clinical presentation of systemic hypertension in WBS children, its origin and management. We included 41 children with confirmed WBS who were referred to the paediatric nephrology or cardiology unit for hypertension.

Results. The mean age at diagnosis of hypertension was 4.7 years. Out of 41, 24 patients had systolic blood pressure (BP) between +10 and +30 mmHg above the 95th percentile (1.645 SD), and 20/41 patients had diastolic BP between the 95th percentile (1.645 SD) and >10 mmHg. Thirty-nine patients were asymptomatic. Arteriography, performed in 17/41 patients, revealed a renal artery stenosis (RAS) in 10 patients (58%). Echocardiography was performed in all patients and showed isthmic coarctation in four patients (9%). Calcium channel blockers were used in half of the patients (22/41) and seemed to control hypertension in most cases. Interventional treatment of RAS was performed in five patients (three angioplasty and two surgical bypass). It controlled hypertension in one patient but remained ineffective in the four others.

Conclusions. Medical treatment essentially calcium blockers improved hypertension in most cases. Interventional treatment of RAS has not been encouraging.

Objectives. To review use of RIFLE and AKIN as AKI trial outcome variables and contrast these with outcomes for CIN.

Methods. We conducted a search of PubMed from 1 January 2005 to 31 December 2008 and 9 trial registries for randomized control trials for preventional or interventional treatment of AKI and CIN.

Results. RIFLE or AKIN were outcome variables in 36% (n = 8) of the published (n = 22) and 18% (n = 4) of the current (n = 22) AKI trials. RIFLE was used to triage to intervention in three trials. The urine output definition of RIFLE and AKIN was an outcome in only two trials. In 18% (n = 8) of AKI trials, the CIN definition (increase in serum creatinine of ≥25% and/or ≥44 µmol/l) was the primary outcome. This was also the primary outcome in 56% (n = 13) of published (n = 12) and current (n = 11) CIN trials. Three published CIN trials used RIFLE or AKIN as an outcome (13%). The duration over which outcomes were determined varied from 24 h to 7 days.

Conclusions. Considerable heterogeneity remains in outcome variables of AKI and CIN clinical trials. Even when the RIFLE or AKIN criteria were used, they were not applied consistently. There is a need for further consensus on surrogate outcome variables.

Methods. Twenty-three (23) patients with IMGN and superimposed FSGS were compared to 35 patients with IMGN alone with respect to the clinical and laboratory features, light microscopic findings and stereologic parameters (glomerular cross-sectional area and estimated glomerular volume).

Results. In the clinical parameters, patients with IMGN-FSGS had a significantly higher incidence of hypertension, raised serum creatinine and microscopic haematuria. The mean 24-h urinary protein excretion was higher in the group with IMGN-FSGS (7.4 ± 1.36 g) as compared to IMGN alone (3.85 ± 0.7 g, P < 0.001, Mann–Whitney test). On light microscopy, biopsies with IMGN-FSGS frequently had mesangial hypercellularity and more extensive tubulo-interstitial disease than those with IMGN alone. Stereological analysis showed that the non-sclerosed glomeruli in biopsies with IMGN-FSGS had a higher mean cross-sectional area (185466.7 ± 32493.3 µ²) and higher estimated volume (855200 ± 152640 µ³) as compared to glomeruli in cases with IMGN alone (76000 ± 14719.2 µ² and 576666.7 ± 131233.3 µ³, respectively).

Conclusion. The present study is probably the first systematic analysis of stereologic parameters in renal biopsies of IMGN with FSGS. Our results objectively demonstrate the glomerular enlargement in the non-sclerosed glomeruli in cases of IMGN with FSGS. This detection of enlarged glomeruli may serve to alert the renal pathologist to the possibility of coexisting FSGS, which is a poor prognostic factor in IMGN.

Methods. We measured fluid overload (FO) prior to a mid-week HD session in 370 randomly selected HD patients (50% with diabetes) from five dialysis centres. A new bioimpedance spectroscopy (BIS) device that implies a validated body composition model was applied. This tool allows correct quantification of extracellular FO or – deficiency in comparison to a healthy reference population (normal range –1.1 to 1.1 L according to the 10th and 90th percentile of measurements). In addition, weight and blood pressure were recorded before and after treatment.

Results. Pre-dialytic FO ranged from –0.5 to 4 L and post-dialytic FO from –2.5 to 2 L (10th and 90th percentile of measurements), indicating that on average the hydration status of healthy subjects is considered as the optimal target weight in HD patients. Comparison of FO between diabetic and non-diabetic patients revealed no difference. Based on the consideration that an FO < –1.1 L before and >1.1 L after HD indicates inadequate DWA, we identified 98 (26%) patients who might benefit from correction of target body weight.

Conclusion. BIS is an interesting, objective method to support clinical DWA. Further studies should be performed to investigate beneficial clinical effects of this approach.

Methods. Linear regression was used to relate log-measured GFR (mGFR) to sex, race, diabetes, transplant, weight, various transformations of creatinine and age with and without interactions. Equations were developed in a pooled database of 10 studies [2/3 (N = 5504) for development and 1/3 (N = 2750) for internal validation], and final model selection occurred in 16 additional studies [external validation (N = 3896)].

Results. The mean mGFR was 68, 67 and 68 ml/min/ 1.73 m² in the development, internal validation and external validation datasets, respectively. In external validation, an equation that included a linear age term and spline terms in creatinine to account for a reduction in the magnitude of the slope at low serum creatinine values exhibited the best performance (bias = 2.5, RMSE = 0.250) among models using the four basic predictor variables. Addition of terms for diabetes and transplant did not improve performance. Equations with weight showed a small improvement in the subgroup with BMI <20 kg/m².

Conclusions. The CKD-EPI equation, based on creatinine, age, sex and race, has been validated and is more accurate than the MDRD study equation. The addition of weight, diabetes and transplant does not significantly improve equation performance.

Methods. The lack of data from randomised controlled trials caused us to conduct the first prospective, randomised, multicentre study on late steroid withdrawal among paediatric kidney allograft recipients treated with standard-dose cyclosporine microemulsion (CsA) and mycophenolate mofetil (MMF) for 2 years. Forty-two low- or regular-immunologic risk patients were randomly assigned, ≥1 year post-transplant, to continue taking or to withdraw steroids over 3 months.

Results. Two years after steroid withdrawal, they showed a longitudinal growth superior to controls [mean height standard deviation score (SDS) gain, 0.6 ± 0.1 SDS versus –0.2 ± 0.1 SDS (P < 0.001)]. The prevalence of the metabolic syndrome declined significantly (P < 0.05), 2 years after steroid withdrawal, from 39% (9/23) to 6% (1/16). Steroid-free patients had less frequent arterial hypertension (50% versus 93% (P < 0.05)) and required fewer antihypertensive drugs [0.6 ± 0.2 versus 1.5 ± 0.3 (P < 0.05 versus control)]. Additionally, they had a significantly improved carbohydrate and lipid metabolism with fewer hypercholesterolaemia and hypertriglyceridaemia (P < 0.05 versus control). Patient and graft survival amounted to 100%. Allograft function remained stable 2 years after steroid withdrawal. The incidence of acute rejections was similar in the steroid-withdrawal group (1/23, 4%) and controls (2/19, 11%).

Conclusion. Late steroid withdrawal in selected CsA- and MMF-treated paediatric kidney transplant recipients improves growth, mitigates cardiovascular risk factors and reduces the prevalence of the metabolic syndrome, at no increased risk of acute rejection or unstable graft function.

Methods. The pregnancy dams were divided in two groups: with normal protein diet (pups named NP) (17% protein) or low protein diet (pups LP) (6% protein) during all pregnancy.

Results. The present data confirm a significant enhancement in arterial pressure in the LP group. Furthermore, the study showed a significantly decreased expression of RAS pathway protein and Ang II receptors in the kidney and an increased expression in the adrenal of LP rats. The detailed immunohistochemical analysis of RAS signalling proteins in the kidney confirm the immunoblotting results for both groups. The present investigation also showed a pronounced decrease in fractional urinary sodium excretion in maternal protein-restricted offspring, compared with the NP age-matched group. This occurred despite unchanged creatinine clearance.

Conclusions. The current data led us to hypothesize that foetal undernutrition could be associated with decreased kidney expression of AT_R resulting in the inability of renal tubules to handle the hydro-electrolyte balance, consequently causing arterial hypertension.

Methods. The aim of this prospective trial was to guide the patient population of a complete dialysis centre towards normohydration over the course of approximately 1 year. Fluid status was assessed frequently (at least monthly) in haemodialysis patients (n = 52) with the body composition monitor (BCM), which is based on whole body bioimpedance spectroscopy. The BCM provides the clinician with an objective target for normohydration. The patient population was divided into three groups: the hyperhydrated group (relative fluid overload >15% of extracellular water (ECW); n = 13; Group A), the adverse event group (patients with more than two adverse events in the last 4 weeks; n = 12; Group B) and the remaining patients (n = 27; Group C).

Results. In the hyperhydrated group (Group A), fluid overload was reduced by 2.0 L (P < 0.001) without increasing the occurrence of intradialytic adverse events. This resulted in a reduction in systolic blood pressure of 25 mmHg (P = 0.012). Additionally, a 35% reduction in antihypertensive medication (P = 0.031) was achieved. In the adverse event group (Group B), the fluid status was increased by 1.3 L (P = 0.004) resulting in a 73% reduction in intradialytic adverse events (P < 0.001) without significantly increasing the blood pressure.

Conclusion. The BCM provides an objective assessment of normohydration that is clinically applicable. Guiding the patients towards this target of normohydration leads to better control of hypertension in hyperhydrated patients, less intradialytic adverse events and improved cardiac function.

Methods. Eight VDR single-nucleotide polymorphisms (SNPs) rs10735810 FokI C>T, rs1544410 BsmI G>A, rs7975232 ApaI G>T, rs731236 TaqI T>C, rs4303288 G>T, rs11168275 C>T, rs12721366 G>A and rs2544043 G>C were investigated with CYP27B1 rs4646536 T>C and CYP2R1 rs10741657 G>A. Genotyping was performed using pyrosequencing, Taqman, Sequenom or direct sequencing technologies in 1329 type 1 diabetics (655 nephropaths, 674 non-nephropaths).

Results. No significant differences were observed in genotype or allele frequencies between case and control groups for VDR, CYP27B1 or CYP2R1 SNPs, either before or after stratification by recruitment centre or when restricted to patients with end-stage renal disease. A previously identified haplotype block from rs1544410 to rs731236 was confirmed at the 3'-end of VDR. Comparison of haplotype frequencies identified the rare AGT haplotype as significantly protective against DN, 3.1% cases versus 5.8% controls; ² = 11.05, Pc = 0.009 by the permutation test.

Conclusions. Our study has identified a rare VDR haplotype that is protective against DN in patients with type 1 diabetes. Replication in a large, independent cohort is required to confirm this finding.

Methods. We selected 57 718 people who had undergone a routine health check-up.

Results. The average CKD awareness was 3.1% (95% CI: 2.6–3.7%) and was increased with progressing CKD stage. The awareness was increased from 1.1% before the WKD campaign to 5.8% after the campaign (P < 0.001). CKD awareness in the post-WKD period was increased in CKD stages 2 (OR 4.535: 95% CI: 2.044–10.062) and 3 (OR 6.614: 95% CI: 4.282–10.217) and profoundly increased in stage 4 (OR 13.800: 95% CI: 2.127–89.524), compared to the pre-WKD period. In the CKD-aware group compared to the CKD-unaware group, the awareness of diabetes mellitus (90.0% versus 54.2%, P < 0.001) and hypertension (87.2% versus 64.7%, P < 0.001) was higher and the levels of systolic blood pressure (116.9 ± 1.0 versus 120.1 ± 0.2, P < 0.01) and serum cholesterol (198.3 ± 2.7 versus 205.0 ± 0.5, P < 0.05) were lower by covariance analysis.

Conclusions. The WKD campaign had a positive impact on the awareness and control of risk factors in CKD subjects but the absolute frequency of CKD awareness still remains undesirable in Korea. We need new campaign strategies to publicize the importance of early diagnosis and appropriate management of CKD.

Methods. One hundred and seven patients with biopsy-proven chronic IgA nephropathy (71 males, 36 females aged 45 ± 11 years) performed a graded exercise treadmill stress test. HRR was measured as the heart rate difference between the peak value and the heart rate 1 min after exercise. The patients were divided into three groups based on estimated glomerular filtration rate (eGFR): CKD 1, eGFR ≥ 90 ml/min (n = 46); CKD 2, eGFR 60–89 ml/min (n = 38), CKD 3–4, eGFR 15–59 ml/min (n = 23). We compared these data with 29 normal controls (aged 46 ± 14 years).

Results. HRR values corresponded to eGFR as follows: 29.9 ± 8.8 bpm normal controls, 27.8 ± 9.2 bpm CKD 1, 24.5 ± 10.5 bpm CKD 2 and 16.3 ± 9.3 bpm CKD 3–4. The latter differed from the other groups significantly (P < 0.05). Metabolic syndrome was common in IgA nephropathy patients (27%). Metabolic syndrome patients had a HRR of 19.6 ± 10.1 bpm, compared to 25.8 ± 10.4 bpm in patients without metabolic syndrome (P = 0.007). Nevertheless, a multivariate regression analysis accepted only eGFR as an independent predictor of HRR.

Conclusion. eGFR predicts HRR in patients with a homogenous renal disease. Metabolic syndrome influences HRR, albeit not independently in this cohort.

Method. The study subjects included 106 stable non-diabetic PD patients who had been on PD for >3 months. We measured baseline characteristics, blood pressure, fasting blood glucose, lipid profiles and high-sensitivity CRP (hsCRP), and defined metabolic syndrome using the modified National Cholesterol Education Program (Adult Treatment Panel III) criteria. Mortality, technical failure and hospitalization were evaluated during the follow-up period.

Results. Metabolic syndrome was present in 50 patients (47.2%), and these showed higher baseline hsCRP levels (0.67; 95% CI: 0.50–0.94 versus 1.78 mg/dl; 95% CI: 1.21–2.57; P < 0.001). Patients with metabolic syndrome experienced significantly lower 5-year survival rates than patients without (90% versus 67%, P = 0.02), although these groups did not differ in peritonitis rates, technical failure or hospitalization. A Cox proportional hazards analysis identified the following as predictors of mortality: metabolic syndrome (RR: 3.39; 95% CI: 1.16–9.94; P = 0.02), baseline albumin (RR: 0.06; 95% CI: 0.01–0.30; P = 0.001) and baseline hsCRP levels (RR: 1.14; 95% CI: 1.07–1.22; P < 0.001).

Conclusion. Metabolic syndrome is prevalent and is a risk factor influencing long-term survival in non-diabetic PD patients.

Methods. Four hundred consecutive live related renal transplant recipients between April 2001 and September 2004, from this single center, were randomized to receive or not receive INH for 1 year after transplantation.

Results. There were 12 dropouts. Of the remaining 388, 181 recipients received INH for 1 year post-transplant and 207 did not. The primary disease, comorbidities, HLA (human leucocyte antigen) match, immunosuppression, episodes of rejection, the use of anti-rejection agents, a past history of TB in the donor, the recipients and in family members living in same house and a history of TB in the family were factors compared in the two groups. The only significant difference between the two groups was that there was an increased family history of TB in recipients who received INH (P = 0.01). One recipient from the INH group and 16 recipients from the non-INH group developed TB (P = 0.0003). Discontinuation of INH for hepatotoxicity was not required in any patient.

Conclusion. These results provide evidence that the use of INH following renal transplantation should be considered mandatory in geographical areas where the prevalence of TB is high. Furthermore, these results have important implication in patients from such areas who are immunosuppressed following other kinds of transplantation and for those who are immunocompromised for any other reason.

The objective of this study was to evaluate the efficacy of peritoneal dialysis (PD) in the treatment of refractory HF in terms of functional status, hospitalization and mortality. We also determined the improvement in health-related quality of life with the use of PD, and examined the economic consequences of its use.

Methods. We conducted a single centre, prospective, non-randomized study involving patients showing symptoms and signs of congestive HF refractory to maximum tolerable drug treatment. All of them were treated with PD. We analysed physical and biochemical determinations, functional status (according to the NYHA classification) and echocardiogram parameters. Also, to determine the efficacy of the technique we compared the perceived state of health (measured by the EQ5D) to PD patients respect to those reported with conservative therapies. Finally, we carried out a cost-utility evaluation measured by the incremental cost-utility ratio between these two options.

Results. Seventeen patients (65% men, 64 ± 9 years) were included in the study, and 12 were still undergoing PD treatment at the end of the follow-up period (15 ± 9 months). All patients improved their NYHA functional status (65% two classes; the rest, one; P < 0.001), with an important improvement in their pulmonary artery systolic pressure (44 ± 12 versus 27 ± 9 mmHg; P = 0.007), but no changes in left ventricular ejection fraction. Hospitalization rates underwent a dramatic reduction (from 62 ± 16 to 11 ± 5 days/patient/year; P = 0.003) before and after PD treatment. PD treatment raised life expectancy of 82% after 12 months of treatment, and 70% and 56% after 18 and 24 months, respectively, much better outcomes than those reported about conservative therapies, which only use diverse diuretic regimens. PD was associated with a higher perception state of health than the conservative therapy (0.6727 versus 0.4305; P < 0.01). Finally, we found that PD is cost-effective compared with the conservative therapy.

Conclusions. We demonstrate that congestive HF programmes should consider offering PD in hope of seeing better functional status, reduced morbidity and mortality, better quality of life as well as reduced health care costs.

Methods. All patients transplanted between July 1972 and March 2007, and followed up at Christchurch Hospital, New Zealand, were studied. Immunosuppression regimens were mostly prednisone, azathioprine, cyclosporine and prednisone, mycophenolate mofetil, cyclosporine since 1998.

Results. Of 384 RTRs, 96 developed at least one NMSC. The median time to first NMSC was 18.3 years (95% CI 14.2, 22.9) from transplant, as estimated by survival analysis. Individual predictors of first NMSC in RTRs were older age at first transplant (P < 0.0001), male sex (P = 0.006) and initial immunosuppression regimen (P = 0.001); only age (P < 0.0001) and male gender (P = 0.003) were significant predictors in a joint model.

The mean rate of subsequent NMSCs was 1.67 per year (95% CI = 1.32, 2.11). Older age at first renal transplant (P = 0.009) or at discovery of the first NMSC (P = 0.01) was associated with a higher annual rate of new NMSC following the discovery of the first NMSC. The median survival time to a second NMSC was 2.2 years (CI 1.4, 3.0). Fourteen patients died of metastatic squamous cell carcinoma (15% case fatality).

Conclusions. NMSCs are a major health issue for RTRs, especially in older males. Once RTRs have developed their first NMSC, ongoing surveillance and prompt treatment are essential.

Methods. To understand the association between MS and CKD, we performed a cross-sectional study in non-institutionalized civilians using the data of the Korean National Health and Nutrition Examination Survey. Of 37 769 participants, 5091 were available for the analysis of the prevalence of CKD (defined as dipstick proteinuria or a reduced GFR < 60 ml/min/1.73 m²).

Results. The prevalence of CKD was 8.9% (7.4% in men, 4.7% in premenopausal women and 20.1% in postmenopausal women) and MS was seen in 26.2% (24.9% in men, 13.9% in premenopausal women and 52% in postmenopausal women). The prevalence of CKD increased with ageing, in particular after sharply after the age of 50 in both genders. MS was a significant determinant of CKD; however, sub-analysis revealed that MS was a risk factor for CKD only in men under the age of 60 and in postmenopausal women. Neither MS per se nor individual components of MS were associated with CKD in men over the age of 60 and in premenopausal women.

Conclusion. Differential effect of MS on CKD according to age and gender in our study may provide a clue to define the subject in need for more attention for the treatment of MS in terms of the development of CKD.

Methods. We retrospectively studied 77 patients with INS and FSGS on native kidneys who underwent renal transplantation. Of these, 42 recipients experienced recurrence of nephrotic range proteinuria.

Results. At time of recurrence, minimal-change disease (MCD) was the main histological feature. On serial biopsies, the incidence of MCD decreased over time, while the incidence of FSGS variants increased. The variant type observed in the native kidneys was not predictive of either recurrence or type of FSGS seen on the allograft. Patients with complete and sustained remission did not developed FSGS.

Conclusion. In conclusion, the Columbia classification is of no help in predicting recurrence after renal transplantation or histological lesions in the case of recurrence of proteinuria.

Methods. We carried out a 3-year, prospective, randomized, controlled clinical multi-centre trial in 156 patients. The patients were randomized to standard treatment (CsA, MMF, steroids) or to high-dose daclizumab (first dose: 2 mg/kg), in combination with low-dose CsA, MMF and steroids. We maintained the mean CsA levels of daclizumab patients at 57% of standard patients (132 versus 216 ng/ml) on Day 7 post-transplant, and 84% by 6 months.

Results. Primary outcome, creatinine clearance (with imputation of informative dropouts) at 12 months, was significantly better in daclizumab-treated (34 ± 17) than standard patients (29 ± 17; P = 0.028, two sided). Only 5 cases of BPAR were recorded in the daclizumab compared to 22 in the standard group (P = 0.0016). Daclizumab patients had 91% event-free survival after 1 year compared to 66% in standard patients (P = 0.00017).

Conclusion. We demonstrate here that high-dose daclizumab in combination with lower CsA levels in adult renal transplant recipients is as or more effective than standard regimen (CsA, MMF, steroids) and may result in better outcomes at 12 months post-transplant with no increase in adverse reactions.

Methods. From 28 patients (mean age 71 years) with various degrees of renal function, over a 24-h period, blood samples were collected every 2 h. An intestinal telemetric sensor was used to measure core temperature. The presence of diurnal rhythms was examined for melatonin, temperature and cortisol. Correlation analysis was performed between Cockcroft–Gault GFR (GFR), melatonin, cortisol and temperature parameters.

Results. The mean GFR was 57 ± 30 ml/min. The subjects exhibited melatonin (n = 24) and cortisol (n = 22) rhythms. GFR was significantly correlated to melatonin amplitude (r = 0.59, P = 0.003) and total melatonin production (r = 0.51, P = 0.01), but not to temperature or cortisol rhythms. Interestingly, no associations were found between the rhythms of temperature, melatonin and cortisol.

Conclusions. As melatonin amplitude and melatonin rhythm decreased with advancing renal dysfunction, follow-up research into circadian rhythms in patients with CKD is warranted.

Methods. We have therefore documented the natural history of all 107 patients referred to a large regional renal unit over a 20-year period and investigated factors associated with survival over a long period of time using Cox regression methods.

Results. Three factors were found to be significantly and independently associated with survival: use of chemotherapy [hazard ratio (HR) 0.21, 95% CI: 0.08–0.46, P < 0.001], serum albumin (HR 0.49, 95% CI: 0.29–0.82, P = 0.02 for ≥35 g/L versus <35 g/L) and dialysis independence (HR 0.43, 95% CI: 0.24–0.76, P = 0.005). However, survival was not found to be better for patients presenting in the second decade compared to the first (HR 0.88, 95% CI: 0.52–1.50, P = 0.65).

Conclusions. This analysis highlights the need for clinical trials of novel chemotherapy regimens in this complicated group of patients. Furthermore, whether strategies to restore or preserve dialysis-independent renal function provide additional benefit to effective chemotherapy also requires further investigation. The advent of efficacious low toxicity chemotherapy (such as thalidomide and bortezomib) and new dialysis techniques to remove free light chains may radically alter the outcome of this group of patients.

Methods. Three hundred and two KTR (216 males and 86 females) were included in this study, and the mean transplant duration was 6.57 years (range 1.5 month–23 years). They were screened for the presence of nail changes. Nail clippings were collected when indicated and cultures were performed for patients with suspected onychomycosis. The patients were compared with 302 age- and sex-matched healthy controls (220 males and 82 females).

Results. One hundred and twenty-one KTR (40.1%) had nail changes compared with 104 (34.4%) in controls. Onychomycosis, Muehrcke's nail and leuconychia were significantly more common in KTR [23 (7.6%), 13.3 (4.3%), 11 (3.6%), respectively] compared with controls [7 (2.3%), 1(0.3%), 2 (0.66%), P = 0.002, 0.001 and 0.02, respectively]. However, the most frequent nail change among KTR and controls was absent lunula, 90 (29.8%) and 80 (26.5%), respectively P = 0.36. Longitudinal ridging was also a frequent nail pathology among KTR and controls, 21 (6.9%) and 19 (6.3%), respectively, P = 0.74.

Conclusion. KTR have higher prevalence rates of onychomycosis, Muehrcke's nail and leuconychia than the healthy population. On the other hand, absent lunula could be a normal variation among Egyptian people.

Methods. Among 183 incident patients, 75 patients finished a complete 36-month protocol. Clinical indices including daily glucose absorption and body composition, by bioelectrical impedance analysis (BIA), were measured in both groups (icodextrin group: 36 patients, non-icodextrin group: 39 patients) at the 1st (baseline), 12th, 24th and 36th months.

Results. There were significant increases in body weight and fat mass during the 36 months after initiation of CAPD. It was found that 78% of 3 years of weight gain occurred during the first year and 88% of weight gain at the end of the first year was fat mass gain. The icodextrin group showed a significantly lower percent of fat mass during the first 36 months (P < 0.05) and also less changes in body weight, fat mass, percent (%) fat mass, visceral fat area and waist/hip ratio at 1, 2 and 3 years than the non-icodextrin group. There were no significant changes in total body water (TBW), extra cellular fluid (ECF), oedema index and lean body mass (LBM) through comparable daily and ultrafiltration volume (UFV) between the two groups during the initial 3 years. Factors associated with the higher percent of fat mass gain over time on peritoneal dialysis were age, diabetes, gender (female) and non-icodextrin group (all, P < 0.01, generalized estimating equation).

Conclusion. The application of icodextrin solution may be a better option to alleviate excessive fat gain over time for patients on PD.

Methods. VSMC proliferation, migration, apoptosis and Runx2 expression were assessed under normal conditions (n = 4) and before and after conversion from CHD to NHD (n = 15).

Results. Compared to normal, CHD is associated with a reduction in VSMC proliferation [0.49 ± 0.07 (CHD) versus 1.34 ± 0.02 RFU, P < 0.01], an augmented caspase-3 activity [0.30 ± 0.02 (CHD) versus 0.22 ± 0.02 RFU, P = 0.014] and a 1.4 ± 0.3 fold increase in Runx2 expression. After conversion to NHD, VSMC proliferation was higher than during CHD [from 0.49 ± 0.07 (CHD) to 0.68 ± 0.09 RFU, P = 0.006] and approached that of controls (1.34 ± 0.02, P > 0.05). Caspase-3 activity was restored to similar values as controls [0.26 ± 0.02 (NHD) versus 0.22 ± 0.04 (normal), P > 0.05]. Runx2 expression decreased to similar levels as normal controls. NHD enhanced dialysis dose delivery, lowered blood pressure, plasma parathyroid hormone levels and normalized plasma phosphate (from 1.7 ± 0.1 to 1.2 ± 0.1 mmol/L, P < 0.01). The reduction in plasma phosphate correlated with the change in VSMC proliferation (r = –0.71, P = 0.007).

Conclusions. We demonstrate that NHD is associated with restoration of abnormal VSMC biology in ESRD. Given the increasing importance of VSMCs in the pathogenesis of atherosclerosis and medial calcification, these data may have important implications for vascular risk in ESRD patients.

Methods. A cross-sectional study with mortality follow-up [median 41 (interquartile range 25–47) months] of haemodialysis patients [n = 173, 100 men, aged 65 (51–74) years]. Abdominal fat deposition was assessed by means of a conicity index (Ci), which estimates fat accumulation in the abdomen as the deviation of body shape from a cylindrical towards a double-cone shape (i.e. two cones with a common base at the waist level). The Ci was studied with regard to baseline inflammatory, anthropometric and nutritional markers, including subjective global assessment (SGA).

Results. Across increasing tertiles of the Ci, patients were older, fatter and more inflamed (P < 0.01 for all). At the same time, they presented a higher prevalence of PEW (SGA >1), reduced handgrip strength and lower S-creatinine (P < 0.01 for all). An increased abdominal fat deposition was associated with worse outcome independently of age, sex, comorbidities and dialysis vintage [Cox HR 1.93 (95% CI = 1.06–3.49)], but the predictive value disappeared following adjustment for interleukin-6 (IL-6) and PEW.

Conclusion. Abdominal fat deposition in haemodialysis patients is linked to both inflammation and PEW, resulting in an increased mortality risk. Our results support the idea that regional differences in adiposity accumulation may have diverse implications on patient outcome.

Methods. A cross-sectional, matched study comparing home haemodialysis (HHD) patients (>15 h/week, n = 28) and conventional haemodialysis (CHD) patients (<15 h/ week, n = 28), matched for age, sex, length of time on dialysis and diabetes, was performed. We measured total body protein (TBP) by in vivo neutron activation, total body fat (TBF) and skeletal muscle mass (SKMM) by dual-energy x-ray absorptiometry (DEXA) and biochemical and inflammatory parameters. Visceral (VFA) and subcutaneous fat areas (SFA) were determined from computed tomography.

Results. There was no significant difference in TBP (10.2 ± 1.9 kg CHD versus 10.8 ± 1.8 kg HHD, P = 0.18) or SKMM (25.6 ± 5.6 kg CHD versus 26.2 ± 4.2 kg HHD). TBF was not different (27.7 ± 10.7 kg CHD versus 27.8 ± 16.0 kg HHD), although the HHD group had greater VFA (182.0 ± 105.6 cm² versus 173.8 ± 90.1 cm²) and lower SFA (306.7 ± 176.4 cm² versus 309.7 ± 138.1 cm²), the difference was not statistically significant. Albumin concentrations were significantly increased in the HHD group (37.5 ± 3.56 g/L versus 35.18 ± 4.11 g/L, P = 0.03), whilst phosphate concentrations (1.57 ± 0.41 mmol/LHHD versus 1.92 ± 0.62 mmol/ LCHD, P = 0.02) and inflammatory parameters were lower. There was a positive relationship between hours of dialysis and TBP (β = 0.08; P = 0.03).

Conclusion. Surrogate nutritional markers and inflammatory parameters improved with more intensive dialysis, but this was not reflected by improved body composition. Further prospective studies are required to confirm whether more intensive dialysis affects body composition, and whether this impacts on metabolic risk and clinical outcome.

Methods. We conducted a cross-sectional and retrospective study in 158 adults who received myeloablative allogeneic HCT for lymphohaematologic malignancies at least 3 years ago and are alive today. The mean survival time was 6.15 ± 4.88 years (range: 3–16 years). CKD was defined as a sustained decrease in glomerular filtration rate (GFR) or persistent proteinuria for a period more than 3 months. GFR was calculated based on serum creatinine (Cr) using the Modification of Diet in Renal Disease formula. Serum Cr and proteinuria were measured at least on three occasions separated by one or more months before the investigation. CKD was classified according to the National Kidney Foundation CKD staging. Proteinuria was defined as positive dipstick test ≥1+. The factors associated with the presence of CKD with a decrease of GFR (CKD ≥ stage 3) were examined using multivariate logistic regression analysis, adjusted for demographic and clinical characteristics.

Results. The prevalence of proteinuria was found in 36 out of 158 patients (22.8%). The prevalence of each CKD stage was as follows: Stage 0 (no CKD), 98 patients (62.0%); Stage 1, 18 patients (11.4%); Stage 2, 15 patients (9.5%); Stage 3, 8 patients (5.1%); Stage 4, 10 patients (6.3%) and Stage 5, 9 patients (5.7%). Initiation of chronic dialysis treatment or transplant was performed in seven CKD stage-5 patients (4.4%) at a mean of 10.9 ± 3.72 years after HCT. Multivariate analysis identified acute kidney injury with HCT [odds ratio (OR), 9.920; 95% confidence interval (CI), 2.084–39.68; P = 0.0051], hypertension after HCT (OR, 4.031; 95% CI, 1.044–13.06; P = 0.0346) and survival time after HCT (OR, 4.275; 95% CI, 2.823–23.04; P = 0.0481) as significant factors associated with the presence of CKD ≥ stage 3.

Conclusions. A remarkably high percentage of long-term survivors had evidence of proteinuria and all stages of CKD. CKD in transplant recipients may result from incomplete recovery from acute renal insults, hypertension and increasing longevity. The CKD cohort should be at a great risk for end-stage renal disease and cardiovascular morbidity and mortality. The burden of CKD should be recognized as a significant public health problem.

Methods. In this observational study, 333 patients (age 67 ± 15 years, 46% diabetics) were included during a 7.5-year period. The mean follow-up was 30 ± 18 months (range 4–79). The influence of study variables was evaluated applying a time-dependent Cox model and slope-based outcome using a linear regression model.

Results. The diabetes condition was associated with adverse outcome in univariate analysis, and after adjusting for age, sex and systolic blood pressure. However, when controlling for albuminuria (a time-dependent covariate), diabetes did not show any association with outcome. In addition, the mean slope of renal decline was similar in diabetic and non-diabetic patients when controlling for albuminuria. The urinary albumin–creatinine ratio was a robust predictor of poor outcome in uni- and multivariate models. In the diabetic group, time-varying glycosilated haemoglobin did not influence renal outcome in the Cox model, and time-varying albuminuria remained a strong predictor of outcome.

Conclusions. Diabetic patients have a poorer renal outcome, but at comparable levels of albuminuria renal decline is similar in diabetic and non-diabetic patients. Albuminuria is a risk factor for renal decline, and the main target to delay progression in patients, diabetics or non-diabetics, with moderate to advanced CKD.

Methods. Potential role of TGF-β signalling in acute peritonitis was investigated in a rat model by infecting peritoneum with E. coli and in primary culture of peritoneal mesothelial cells (PMC) by LPS.

Results. We found that a single infection of E. coli caused an acute, but transient peritonitis by a significant increase in ascites white blood cells (WBC), peritoneal CD45+ leukocytes, upregulation of TNF, activation of NF-B/p65 and impaired peritoneal function (all P < 0.01). Interestingly, spontaneous recovery of acute peritonitis occurred with upregulation of TGF-β1 and activation of Smad2/3, suggesting a protective role of TGF-β signalling in acute peritonitis. This was demonstrated by the finding that blockade of the TGF-β signalling pathway with gene transfer of Smad7 inactivated peritoneal Smad2/3 but worsened E. coli-induced, NF-B-dependent peritoneal inflammation and peritoneal dysfunction (all P < 0.01). Furthermore, studies in vitro also found that impaired TGF-β signalling by overexpressing Smad7 in PMC were able to overcome the inhibitory effect of TGF-β on LPS-induced, NF-B-mediated peritoneal inflammation.

Conclusion. Results from this study demonstrate that TGF-β signalling is essential in protection against acute peritoneal inflammation induced by bacterial infection.

Methods. Thirty-two male Wistar rats were divided into four groups: control Wistar rats with non-treated (n = 8), streptozotocin (STZ)-induced diabetic rats with 5/6 kidney ablation (n = 8), STZ-induced diabetic rats with 5/6 kidney ablation injected with a standard lactate-buffered 4.25% glucose-based PDF (Dianeal®; n = 8) and STZ-induced diabetic rats with 5/6 kidney ablation injected with 7.5% icodextrin-based PDF (Extraneal®; n = 8). Intraperitoneal injection was performed once daily with an instillation volume of 20 ml per injection during 8 weeks.

Results. Chronic high-glucose-based PDF exposure resulted in increased vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) expression, accumulation of advanced glycation end-products (AGEs), and up-regulation of the receptor for AGE (RAGE), which were ameliorated in the icodextrin-based PDF group. The peritoneal damages, such as neoangiogenesis and submesothelial fibrosis, were significantly reduced in icodextrin-based PDF compared to high-glucose-based PDF.

Conclusions. Long-term in vivo exposure to high glucose-based PDF promotes the fibrosing process of peritoneal membranes. Icodextrin-based PDF may be helpful in slowing the PDF-induced deterioration of peritoneal function and prolonging the use of peritoneal dialysis in patients with diabetes.

Methods. We conducted a single centre, retrospective inception cohort study. Charts were reviewed at presentation (initial renal biopsy), 6-month (follow-up biopsy) and 12-month follow-up.

Results. The population consisted of 21 patients (median age, 14.5 years): 19/21 were female, 6/21 African American, 3/21 Asian, 9/21 Caucasian and 3/21 Hispanic. At presentation, 19/21 had elevated aCL, 15/21 hypertensive, 12/21 nephrotic and 7/21 required haemodialysis (HD)—2/7 HD patients had thrombotic microangiopathy, 1/7 crescentic glomerulonephritis. Two patients had thromboembolism: both had aCL, were taking oral contraceptives and required HD, one was nephrotic and the other had elevated lupus anticoagulant. Initial biopsies revealed 6/21 ISN/RPS class II nephritis, 3/21 class III, 7/21 class IV and 5/21 class V. Treatment consisted of methylprednisolone, corticosteroids, cyclophosphamide or mycophenolate mofetil. Follow-up biopsies revealed 12/13 to have improved histology. Indication for a follow-up biopsy was severe illness at presentation. At 12-month follow-up, no patients were nephrotic (P < 0.001) or required HD (P < 0.001), and 3/14 had elevated aCL (P < 0.001).

Conclusion. Elevated aCL, hypertension, nephrotic syndrome and need for HD were common presentations among our paediatric SLE nephritis population. Renal histology and aCL were helpful in the therapeutic management.

Methods. The expression of -DG and sialidase was investigated by immunofluorescence in kidney biopsies of patients with MCN (n = 5), FSGS (n = 15), proliferative lupus nephritis (LN, n = 9), membranous glomerulopathy (MG, n = 10) and normal human kidneys (NHK, n = 4). The urinary sialic acid concentration was measured using a newly developed LC-tandem mass spectrometry method.

Results. A 3-fold increased glomerular expression of sialidase was found in MG, accompanied with an increased urinary sialic acid concentration in two MG patients. However, we did not observe major changes in the expression of -DG in patients with the above-mentioned glomerular diseases compared to NHK, also not between MCN and FSGS.

Conclusions. Endogenous glomerular sialidase expression is increased in MG, which might represent a novel mechanism for the loss of negative charge in the glomerular capillary filter. The expression of dystroglycan cannot be used as a diagnostic tool to differentiate between glomerular diseases.

Methods. Thirty-two patients underwent preoperative measurement of small artery elasticity index, and pre-anastomosis measurement of artery and vein luminal diameters during fistula surgery. Fistulas were considered mature if they were used successfully in three consecutive treatments within 6 months. A mathematical model was used to determine whether vessel dilatation is needed for adequate fistula flow.

Results. Six fistulas were excluded from analysis of maturation because dialysis did not begin within 6 months. Twenty-one of the remaining 26 fistulas were located in the upper arm. Six of 26 failed to mature, and all 6 developed stenosis. The average small artery elasticity index was lower in failed than in matured fistulas (2.25 versus 3.71 ml/ mmHg x 100, P = 0.02). Artery and vein diameters of the 32 patients ranged from 2.5 to 5.0 and 3.5 to 7.0 mm, respectively. When the diameters were applied to the mathematical model, predicted fistula flows ranged from 412 to 1380 ml/min.

Conclusions. Low arterial elasticity is associated with stenosis and fistula maturation failure. However, vessel dilatation is not needed for adequate blood flow except at the smaller diameters in this study. We speculate that low elasticity promotes development of stenosis. Larger studies are needed to confirm these promising results and to determine whether therapies directed at improving elasticity can improve maturation.

Methods. A multicentre prospective observational cohort study was performed in four teaching hospital renal units serving a total population of four million people. A total of 884 consecutive patients treated with renal replacement therapy were studied. Cox proportional hazard modelling and adjusted survival curves were used to assess the impact of a range of variables on patients surviving dialysis for more than 90 days. Further analysis was undertaken to determine the likelihood of transplantation in different ethnic groups.

Results. Survival was 29% after a mean and median follow up of 4.6 and 4.2 years, respectively. Factors associated with worse survival included the following: age; for each decade of life the relative risk (RR) of death was 1.52 (95% confidence intervals 1.41–1.65, p < 0.0001); comorbidity, one or two comorbid conditions, RR = 1.56 (95% CI 1.24–1.95, p < 0.001) and three or more comorbid conditions, RR = 2.34 (1.68–3.27, p < 0.001). Factors associated with better survival included the following: south-Asian ethnicity, RR = 0.6 (0.46–0.80, p < 0.001); renal transplantation, RR = 0.20 (95% CI 0.11–0.59, p < 0.0001) and glomerulonephritis as the primary renal disease, RR = 0.70 (0.50–0.97, p = 0.04). Factors associated with likelihood of transplantion were having a functioning fistula/peritoneal dialysis catheter at start of dialysis (RR 1.91, 95% CI 1.24–2.94, p = 0.003) and glomerulonephritis (RR 9.54, 95% CI 2.43–37.64, p = 0.001). Patients were less likely to receive if they were black (RR 0.10, 95% CI 0.02–0.34, p < 0.001), South Asian (RR 0.64, 95% CI 0.42–0.97, p = 0.037), diabetic (RR 0.06, 95% CI 0.01–0.23, p < 0.001) and had one or two comorbid conditions (RR 0.51, 95% CI 0.32–0.82, p = 0.06). Every decade increase in age was also associated with a lesser likelihood of transplantation (RR 0.55, 95% CI 0.49–0.61, p < 0.001).

Discussion. Risk stratification at commencement of chronic dialysis may predict long-term survival in different patient groups. As expected ethnic minorities are less likely to receive a transplant and this should be addressed by the new waiting list prioritization. The better survival on dialysis in this population of patients with south-Asian ethnicity is unexplained and this requires further investigation.

Methods. Two types of polyethersulfone membranes only differing in albumin permeability (referred as PU– and PU+) were compared in eight patients on maintenance dialysis in a prospective cross-over manner. Treatment settings were identical for individual patients: time 229 ± 22 min; blood flow rate 378 ± 33 mL/min; dialysate flow rate 500 mL/min; substitution flow rate in haemodiafiltration 94 ± 9 mL/min. Removal of the protein-bound compounds p-cresyl sulfate (pCS) and indoxyl sulfate (IS) was determined by reduction ratios (RRs), dialytic clearances and mass in continuously collected dialysate. In addition, the elimination of the low-molecular weight (LMW) proteins beta₂-microglobulin, cystatin c, myoglobin (myo), free retinol-binding protein (rbp) and albumin was measured.

Results. Plasma levels of the protein-bound toxins were significantly decreased by all treatment forms. However, the decreases were comparable between dialysis membranes and between haemodialysis and haemodiafiltration. The RRs of total pCS ranged between 40.4 ± 25.3 and 47.8 ± 10.3% and of total IS between 50.4 ± 2.6 and 54.6 ± 8.7%. Elimination of free protein-bound toxins as assessed by their mass in dialysate closely correlated positively with the pre-treatment plasma concentrations being r = 0.920 (P < 0.001) for total pCS and r = 0.906 (P < 0.001) for total IS, respectively. Compared to haemodialysis, much higher removal of all LMW proteins was found in haemodiafiltration. Dialysis membrane differences were only obvious in haemodialysis for the larger LMW proteins myo and rbp yielding significantly higher RRs for PU+ (myo 46 ± 9 versus 37 ± 9%; rbp 18 ± 5 versus 15 ± 5%; P < 0.05). Additionally, the albumin loss varied between membranes and treatment modes being undetectable with PU– in haemodialysis and highest with PU+ in haemodiafiltration (1430 ± 566 mg).

Conclusions. The elimination of protein-bound compounds into dialysate is predicted by the level of pre-treatment plasma concentrations and depends particularly on diffusion. Lacking enhanced removal in online post-dilution haemodiafiltration emphasizes the minor significance of convection for the clearance of these solutes. Compared to LMW proteins, the highly protein-bound toxins pCS and IS are less effectively eliminated with all treatment forms. For a sustained decrease of pCS and IS plasma levels, alternative strategies promise to be more efficient therapy forms.

Methods. The authors pooled individual-level cross-sectional data from 18 253 persons aged 28–100 years in four studies: the Cardiovascular Health Study; the Health, Aging and Body Composition Study; the Multi-Ethnic Study of Atherosclerosis and the Prevention of Renal and Vascular End-Stage Disease cohort. Kidney function was measured by cystatin C. Clinical risk factors for kidney disease included diabetes, hypertension, obesity, smoking, coronary heart disease, cerebrovascular disease, peripheral arterial disease and heart failure.

Results. Across the age range, there was a strong, non-linear association of age with cystatin C concentration. This association was substantial, even among participants free of clinical risk factors for kidney disease; mean cystatin C levels were 46% higher in participants 80 and older compared with those <40 years (1.06 versus 0.72 mg/L, P < 0.001). Participants with one or more risk factors had higher cystatin C concentrations for a given age, and the age association was slightly stronger (P < 0.001 for age and risk factor interaction).

Conclusions. There is a strong, non-linear association of age with kidney function, even in healthy individuals. An important area for research will be to investigate the mechanisms that lead to deterioration of kidney function in apparently healthy persons.

Methods. Male SHR and Wistar-Kyoto rats (WKY) were divided into eight groups: normal-fat diet-fed WKY (WKY-NF), high-fat diet-fed WKY (WKY-HF), high-fat diet-fed tempol-treated WKY (WKY-HF/T), high-fat diet-fed candesartan-treated WKY (WKY-HF/C), normal-fat diet-fed SHR (SHR-NF), high-fat diet-fed SHR (SHR-HF), high-fat diet-fed tempol-treated SHR (SHR-HF/T) and high-fat diet-fed candesartan-treated SHR (SHR-HF/C). After 12 weeks of treatment, haemodynamic measurements and histological assessment of the kidney were performed.

Results. At the end of week 12, the high-fat fed SHR gained more body weight, their systolic blood pressure was further elevated and glucose intolerance induced. There was no significant difference in the insulin resistance index, serum lipid profile, plasma renin activity and serum aldosterone levels according to diet. However, the high-fat diet resulted in increases in immunohistochemical stains of renin and angiotensin II in the kidney. The real-time PCR also demonstrated significant increases in mRNA levels of renin, angiotensinogen and angiotensin-converting enzyme in the kidney, reflecting enhanced activation of the intrarenal RAS, which findings were also shown by Western blot analysis for renin and angiotensin II type 1 receptor. The expression of ED-1, osteopontin and TGF-β1 in the renal cortex were prominently enhanced in the SHR-HF group with the increased intrarenal lipid concentrations and oxidative stress. Administration of tempol or candesartan in the high-fat diet-induced SHR inhibited the elevation of the systolic blood pressure, intrarenal lipid concentrations, oxidative stress and the degree of renal inflammation to the levels of, or more than, the SHR-NF with no differences in the body weight and periepididymal fat weight, compared to those in the SHR-HF group without such treatment.

Conclusions. Our study suggests that a high-fat diet induces fatty kidneys, aggravation of blood pressure and renal inflammation in the SHR. Blockade of oxidative stress by tempol or of RAS by candesartan ameliorates the increase in blood pressure and renal inflammation and improves intrarenal lipid accumulation. Therefore, antioxidants or angiotensin receptor blockers can prevent diet-induced hypertension and renal inflammation in hypertensive rats.

Methods. An epidemiological cross-sectional study was designed to analyse the prevalence of hypovitaminosis D (‘D’AVIS’ study) in our reference area. The study was performed on a representative random sample of the population over 64 years of age obtained from five primary health care areas. A medical record, arterial BP and biological analysis: serum 25(OH)-D, iPTH, creatinine, urea, calcium, albumin were obtained.

Results. A total of 237 subjects (53% women), aged between 64 and 93 (mean 71.7 ± 5.3), were evaluated. The mean serum 25(OH)-D levels were 17.21 ± 7.57 ng/ml (interval 5–54; 86% had <25 ng/ml). The mean BP was 138.8 ± 14/80 ± 7.4 mmHg, and 46% were on antihypertensive treatment. A significant negative association was observed between serum 25(OH)-D levels and systolic (r = –0.153, P = 0.018) and diastolic BP (r = –0.152, P = 0.019). This association persisted after controlling for possible confounders in the multivariate analyses.

Conclusions. Low serum 25(OH)-D levels were inversely and independently associated with BP. Supplemental measures to prevent hypovitaminosis D in this population would be important, not only to protect the skeletal system but also for the possible beneficial effects on the cardiovascular system and the BP regulation.

Methods. A total of 1495 adults living in the Lorraine region and starting renal replacement therapy from 1997 to 2003 were included. A propensity score (PS) of registration on the renal transplant waiting list was estimated. Patient survival was studied using a time-dependent Cox multivariate regression and a Cox model stratified by PS tertiles. Survival of older patients (≥60 years) was detailed.

Results. Survival was associated with age, medical factors and transplantation. The hazard ratio (HR) of death for patients on dialysis compared to transplant recipients was 4.6 (95% CI: 2.9–7.2). The survival analysis stratified by PS was similar to the multivariate Cox model. The survival benefit of transplantation over dialysis persisted among elderly patients [HR: 4.6 (95% CI: 2.2–9.7)].

Conclusions. In a French community-based network, after taking into account comorbidities, transplantation was associated with longer survival even among elderly patients. Age per se should not therefore be considered as a contraindication to renal transplantation. However, elderly patients should be evaluated carefully before registration on the list. Medical guidelines should put forward a standard set of criteria for access to renal transplantation.

Methods. This retrospective study included 78 consecutive patients from eight dialysis units who were referred to a single interventional radiology centre for endovascular treatment of delayed maturation (n = 30), dysfunction (n = 35) or thrombosis (n = 13) of their autogenous forearm ulnar-basilic (n = 62) or radial-basilic fistulas (n = 16). The male/female ratio was 54/24, mean age was 64.7 years, 26% had diabetes, 83% were treated for hypertension and the mean body mass index was 24 kg/m². Immature and dysfunctional fistulas were treated by dilation and thrombosed fistulas by aspiration thrombectomy. Clinical success was defined as the perception of a continuous palpable thrill and the ability to perform dialysis. Fistula patency rates were calculated with the Kaplan–Meier method.

Results. Overall primary patency rates were 51% and 44% at 1 and 2 years, respectively. These rates were lower for immature and thrombosed fistulas compared to dysfunctional mature fistulas. Secondary patency rates were 96% and 91% at 1 and 4 years, respectively. Immediate overall clinical success was 97%. The two failures occurred with an immature and a thrombosed fistula. Immediate complications included two transient dilation-induced ruptures treated by prolonged balloon inflation. One case of subsequent hand ischaemia was successfully treated by distal artery ligation.

Conclusions. Endovascular treatment plays a major role in the maturation process, maintenance and salvage of radial and ulnar-basilic fistulas. The preservation of upper arm veins for the future, with low risk of hand ischaemia or hyperflow, might encourage nephrologists and surgeons to consider forearm basilic fistulas systematically in their strategy of vascular access creation.

Methods. We prospectively studied 100 consecutive first renal transplant (RT) receivers. All patients had a preoperative physical examination with a careful vascular system evaluation including assessment of risk factors and colour DUS of aortic, iliac and femoral arteries. Renal transplantation was planned in the right iliac fossa with end-to-lateral vascular anastomoses. Clinical parameters, DUS results, operative and post-operative parameters at 3 months were compared according to the vascular assessment.

Results. Among the 84 patients presenting with a normal preoperative physical arterial examination, 12 patients (14.3%) had an abnormal DUS, revealing atherosclerotic arteries, but no case of arterial stenosis. Among the 16 patients with abnormal physical arterial examination, 10 patients (62.5%) had abnormal DUS, including 4 cases of iliac stenosis. In 3 of the 16 patients (18.8%), DUS revealed right iliac artery stenosis requiring a modification in the surgical procedure. No additional vascular procedure was reported in the case of normal preoperative vascular examination. No technical problems during arterial anastomosis and no post-transplantation arterial complications were reported. In multivariate analysis, abnormal physical examination was the most significant risk factor of atherosclerotic infiltration in DUS.

Conclusion. The abnormality of arterial physical examination is the best clinical predictor of abnormal DUS in preoperative assessment of renal transplant receivers. However, the low sensitivity and positive predictive value of the physical examination do not support the conclusion that DUS can be avoided in patients with normal arterial physical examination. Nevertheless, in the case of arterial physical abnormality, ‘for case’ DUS is critical and helps in the surgical strategy in ~20% of cases.

Methods. We analysed 554 hypertensive nephrosclerosis participants (without clinically significant proteinuria) from the longitudinal National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) African American Study of Kidney Disease and Hypertension (AASK) cohort to determine whether decline in glomerular filtration rate (GFR) over ~3.8 years was predicted by common genetic variation within the adrenergic beta-1 (ADRB1) receptor at non-synonymous positions Ser49Gly and Arg389Gly.

Results. The polymorphism at Ser49Gly (though not Arg389Gly, in only partial linkage disequilibrium at r² = 0.18) predicted the chronic rate of GFR decline, with minimal decline in Gly₄₉/Gly₄₉ (minor allele) homozygotes compared to Ser₄₉ carriers; concordant results were observed for haplotypes and diploid haplotype pairs at the locus. An independent replication study in 1244 subjects from the San Diego Veterans Affairs Hypertension Cohort confirmed that Gly₄₉/Gly₄₉ homozygotes displayed the least rapid decline of eGFR over ~3.6 years.

Conclusion. We conclude that GFR decline rate in hypertensive renal disease is controlled in part by genetic variation within the adrenergic pathway, particularly at ADRB1. The results suggest novel strategies to approach the role of the adrenergic system in the risk and treatment of progressive renal disease.

Methods. Given the phenotype of Tshz3 mutant mice, we considered that Teashirt genes, which code for a family of transcription factors, might represent candidate genes for human PUJO. To evaluate this possibility, we used in situ hydridization to analyse the three mammalian Tshz genes in mouse embryonic ureters and determined whether TSHZ3 was expressed in the human embryonic ureter. TSHZ2 and TSHZ3 were sequenced in index cases with non-syndromic PUJO.

Results. Tshz2 and Tshz3 genes were detected in mouse ureters and TSHZ3 was expressed in the human embryonic renal pelvis. Direct sequencing of TSHZ2 and TSHZ3 did not identify any mutations in an initial cohort of 48 PUJO index cases, excluding these genes as a major cause of this condition. A polymorphic missense change (E469G) in TSHZ3 was identified at a residue highly conserved throughout evolution in all Teashirt proteins, although subsequently no significant difference between the E469G allele frequency in Albanian and Macedonian PUJO index cases (3.2%) versus 633 control individuals (1.7%) was found (P = 0.18).

Conclusions. Mutations in TSHZ2 and TSHZ3 are not a major cause of PUJO, at least in Albanian and Macedonian populations. Expression of these genes in the human fetal ureter emphasizes the importance of analysing these genes in other groups of patients with renal tract malformations.

Methods. Male mice were subjected to bilateral renal ischaemia for 30 min and reperfusion for 24 h, or to a sham operation. Both the IRI group and the sham group were intravenously injected with an adenovirus harbouring the mouse Klotho gene (ad-kl) before renal IRI. In addition, mIMCD3 cells induced to overexpress Klotho by transferring the Klotho gene with ad-kl were analysed by DNA microarray and real-time PCR. Renal expression of Klotho and several genes selected by DNA microarray were assessed by real-time PCR or Western blotting, and TUNEL staining was performed to assess apoptosis.

Results. Prior administration of ad-kl to the mice resulted in robust induction of Klotho mRNA in the kidney and liver. Ad-kl transfer improved the plasma creatinine values and mitigated the histological damage and apoptosis induced by IRI. Expression of several genes was altered in mIMCD3 cells as a result of the change in Klotho expression, and expression of heat shock protein 70 (HSP70), in particular, was up-regulated in ad-kl mouse kidneys and HK2 cells.

Conclusion. The results suggest that Klotho is involved in the pathophysiology of IRI. Klotho mitigates apoptosis in experimental ischaemic acute kidney injury via expression of HSP70.

Methods. Using a variable volume two-pool urea kinetic model, we derived clearances based on G [urea nitrogen (UN) generation rate] divided by time-averaged UN (G/TAC), mean predialysis UN (G/meanpre or ‘standard’ Kt/V) or peak UN (G/peak) when identical dialysis treatments were given on a poorly spaced (Monday—Tuesday—Wednesday) versus a well-spaced (Monday—Wednesday—Friday) schedule. We also calculated the ‘gain’ in each clearance when well-spaced treatments were given six versus three times a week. Modelling parameters were diffusive dialyser clearance = 283 ml/min, session length = 210 min (105 min for 6/week), G = 7 mg/min, V = 35 l and weight gain = 10 l/week.

Results. The ‘standard’ Kt/V (G/meanpre) was the same with the poorly spaced (Monday—Tuesday—Wednesday) and well-spaced (Monday—Wednesday—Friday) schedules. In contrast, the G/TAC- and G/peak-based clearances were higher with the well-spaced schedule (+20% and +37%, respectively).

When total treatment time was held constant at 630 min/week, the gain of moving from three to six treatments per week was lower with G/TAC (+9%) than with G/meanpre (+29%) or with G/peak (+18%). When 6/week treatment time was doubled to 1260 min/week, the gains with G/TAC and G/pre (relative to 3/week with 630 min/week dialysis) were similar (about +94% to 97%), but were lower with G/peak (+55%).

Conclusions. All three equivalent clearances increased on moving from three to six sessions per week, with standard Kt/V having the greatest increase. Standard Kt/V is not at all sensitive to spacing. Alternative clearances based on the TAC or peak concentration have the advantage of taking both spacing and frequency into account.

Design, setting, participants and methods. We recruited 61 participants from two dialysis clinics to complete questionnaires regarding dialysis withdrawal preferences in five different health states. Engagement in advance care planning (end-of-life discussions), completion of advance directives and ‘do not resuscitate’ or ‘do not intubate’ (DNR/DNI) orders were ascertained by a questionnaire and from dialysis unit records.

Results. The mean age was 62 ± 15 years; 38% were Black, 11% were Latino, 34% were White and 16% of participants were Asian. Blacks were less likely to prefer dialysis withdrawal as compared with Whites (odds ratio 0.16, 95% confidence interval 0.03–0.88) and other race/ethnicity groups, and this difference was not explained by age, education, comorbidity and other confounders. In contrast, older age was not associated with preferences for withdrawal. Rates of engagement in end-of-life discussions were higher than for documentation of advance care planning for all age and most race/ethnicity groups. Although younger participants and minorities were generally less likely to document treatment preferences as compared with older patients and Whites, they were not less likely to engage in end-of-life discussions.

Conclusions. Preferences for withdrawal vary by race/ ethnicity, whereas the pattern of engagement in advance care planning varies by age and race/ethnicity. Knowledge of these differences may be useful for improving communication about end-of-life preferences and in implementing effective advance care planning strategies among diverse haemodialysis patients.

Methods. Patients with the first relapse of MCNS were randomly assigned to two groups, namely, the CyA (AUC 1700–2000 ng/ml) + PSL (0.8 mg/kg/day) group (n = 26) and the PSL alone (PSL) (1.0 mg/kg/day) group (n = 26), and the clinical characteristics were compared between the two groups. All patients used C2 for CyA monitoring.

Results. A significant decrease of the urinary protein excretion (P = 0.02) and serum total cholesterol (P = 0.003) was observed at 2 weeks from the first relapse in the CyA + PSL group. The increase in the serum total protein (P = 0.03) and serum albumin (P = 0.007) as compared with that in the PSL group was also observed in the CyA + PSL group at this time-point. The time to remission in the CyA + PSL group was shorter than that in the PSL group (P = 0.006).

Conclusion. It was possible to obtain early remission and reduce the PSL dose with combined CyA and PSL therapy in patients with MCNS.

Methods. Adult male Wistar albino rats were assigned to one of six treatment groups: group 1 (control) rats were given daily intraperitoneal (I.P.) injections of normal saline for 8 consecutive days; groups 2, 3 and 4 rats were given GM (80 mg/kg/day, I.P.), l-carnitine (200 mg/kg/day, I.P.) and d-carnitine (250 mg/kg/day, I.P.), respectively, for 8 consecutive days. Rats of group 5 (GM plus d-carnitine) received a daily I.P. injection of d-carnitine (250 mg/kg/day) 1 h before GM (80 mg/kg/day) for 8 consecutive days. Rats of group 6 (GM plus l-carnitine) received a daily I.P. injection of l-carnitine (200 mg/kg/day) 1 h before GM (80 mg/kg/day) for 8 consecutive days.

Results. GM significantly increased serum creatinine, blood urea nitrogen (BUN), urinary carnitine excretion, intramitochondrial acetyl-CoA and total nitrate/nitrite (NOx) and thiobarbituric acid reactive substances (TBARS) in kidney tissues and significantly decreased total carnitine, intramitochondrial CoA-SH, ATP, ATP/ADP and reduced glutathione (GSH) in kidney tissues. In carnitine-depleted rats, GM caused a progressive increase in serum creatinine, BUN and urinary carnitine excretion and a progressive decrease in total carnitine, intamitochondrial CoA-SH and ATP. Interestingly, l-carnitine supplementation resulted in a complete reversal of the increase in serum creatinine, BUN, urinary carnitine excretion and the decrease in total carnitine, intramitochondrial CoA-SH and ATP, induced by GM, to the control values. Moreover, the histopathological examination of kidney tissues confirmed the biochemical data, where l-carnitine prevents and d-carnitine aggravates GM-induced ARF.

Conclusions. (i) GM-induced nephrotoxicity leads to increased urinary losses of carnitine; (ii) carnitine deficiency is a risk factor and should be viewed as a mechanism during the development of GM-induced ARF; and (iii) carnitine supplementation ameliorates the severity of GM-induced kidney dysfunction by increasing the intramitochondrial CoA-SH/acetyl-CoA ratio and ATP production.

Methods. Two weeks after a subtotal nephrectomy, rats received a continuous infusion of dimethyloxalylglycine (DMOG) for 4 weeks to activate HIF.

Results. The DMOG infusion halted the progression of proteinuria. A histological evaluation revealed that the glomerulosclerosis and tubulointerstitial injury were significantly decreased by DMOG treatment. DMOG increased renal HIF-1 protein. The expression of glucose transporter-1 (GLUT-1) and prolyl hydroxylase 3 (PHD3) and the immunostaining of vascular endothelial growth factor (VEGF) were increased by DMOG. DMOG-treated rats showed less podocyte injury manifested by decreased immunostaining of desmin and the restoration of podoplanin staining. Furthermore, plasma malondialdehyde (MDA), a marker of oxidative stress, showed a tendency to decrease, and the renal expression of catalase, an antioxidant, was significantly increased by DMOG. The DMOG treatment decreased macrophage infiltration and reduced fibrosis, as manifested by decreased type IV collagen and osteopontin expression.

Conclusions. Activation of HIF by DMOG halted the progression of proteinuria and attenuated structural damage by preventing podocyte injury in the remnant kidney model. This renoprotection was accompanied by a reduction of oxidative stress, inflammation and fibrosis.

Methods. We investigated 22 patients treated either with a single dose of cisplatin, carboplatin or oxaliplatin. Carnitine and kidney function parameters were determined in plasma and urine. Inhibition and mRNA expression of OCTN2, the principle carnitine transporter, were assessed in L6 cells overexpressing OCTN2 and in 293-EBNA cells, respectively.

Results. Renal excretion of free and short-chain acylcarnitine increased already at the day of administration was maximal the day after and had normalized 1 week after administration of cisplatin, carboplatin or oxaliplatin. The renal excretion fractions for free carnitine and acylcarnitines increased 4–10 times during treatment with platin derivatives. Renal excretions of 1-microglobulin and other proximal tubular markers were also increased, compatible with a proximal tubular defect. Direct inhibition of OCTN2 expressed in L6 cells by cisplatin, oxaliplatin or platinum²⁺ could not be demonstrated, and experiments using urine from patients treated with cisplatin inhibited OCTN2 activity no more than expected from the carnitine content in the respective urine sample. Cisplatin was associated with a time- and concentration-dependent decrease of OCTN2 mRNA and protein expression in 293-EBNA cells.

Conclusions. All platin derivatives investigated are associated with renal tubular damage in humans without significantly affecting glomerular function. The rapid onset and complete reversibility of this effect favour a functional mechanism such as impaired expression of OCTN2 in proximal tubular cells.

Methods. From November 2004 to December 2007, 28 RCFs were created in 28 patients with a distal radial artery internal diameter <1.6 mm using microsurgery and preventive haemostasis. The median age was 68 and the male/female ratio was 6/22. The incidence of age >65 years was 64%, hypertension 96%, diabetes 32.1%, obesity (BMI>30) 35%, vascular disease 46%. The mean distal radial artery and cephalic vein internal diameters, measured with ultrasound examination, were 1.3 mm and 1.9 mm, respectively. Seventy-five percent of the patients were not yet on dialysis treatment; 19% of whom had a previous failed vascular access created elsewhere without microsurgery. The remaining 25% patients were on dialysis treatment with a temporary femoral catheter.

Results. All interventions ended with a patent anastomosis; no thrombosis occurred within the initial 24 h. The early failure rate was 14% (4 out of 28 patients). The causes of early failure were thrombosis >1 week after surgery in one patient, lack of maturation (patent but unfunctional fistula) due to juxta-anastomotic vein stenosis in two patients and mid-vein stenosis in one patient. Treatment for all patients was proximalization of the anastomosis at the distal/mid forearm. Primary patency and secondary patency at 1 year were 68 ± 10% and 96 ± 5%, respectively.

Conclusions. From our findings, we have shown that it is possible to create RCF in adult patients with a radial artery internal diameter of <1.6 mm with an acceptable risk of early failure rate using microsurgery along with preventive haemostasis.

Methods. A total of 120 chronic kidney disease (CKD) stage 5 patients on HD and with the serum phosphorus level >2.1 mmol/l were randomized to receive double-blind treatment with either 3, 6 and 9 g/day MCI-196 or placebo for 3 weeks.

Results. Serum phosphorous decreased in all three treatment groups (–0.038, –0.268 and –0.257 mmol/l in the 3, 6 and 9 g/day groups, respectively). The difference between treatment and placebo groups was significant for the 6 and 9 g/day groups (P < 0.05 in both cases). Changes in the mean serum calcium were minimal and without relevant differences between groups. However, calcium–phosphorus product (Ca x P) was significantly reduced in the 6 and 9 g/day groups P < 0.05). MCI-196 at all doses decreased serum intact PTH between baseline and endpoint, and differences between treatment groups and placebo were statistically significant for the 3 and 9 g/day groups (P < 0.02 in both cases). Both serum total and LDL cholesterol decreased significantly in all treatment groups compared to placebo (by 0.71–1.05 mmol/l, for total cholesterol and 0.68–0.94 mmol/l for LDL cholesterol P < 0.001 in all cases). There was minimal change in serum HDL cholesterol. MCI-196 at all doses decreased significantly serum uric acid between baseline and endpoint compared to placebo (P < 0.005 in all cases). The drug was well tolerated.

Conclusion. MCI-196 significantly reduced serum phosphorus, Ca x P and PTH, without effecting serum calcium levels. The additional reduction in total cholesterol and LDL cholesterol indicates a possible dual mechanism of action of MCI-196 that has the potential to reduce cardiovascular morbidity in CKD stage 5 patients.

Methods. A total of 25 Caucasian patients (14 male, median age 44.2 ± 9.2 years, BMI 23.7 ± 4.0 kg/m²) were assessed in a prospective trial before, 1, 3 and 12 months after RTx from living donors by clinical examination, cardiopulmonary exercise testing, dual X-ray absorptiometry (DEXA) and analysis of plasma indices.

Results. Creatinine clearance improved from 8.0 ± 3.1 to 60.9 ± 18.1 mL/min at 1 month, but declined at 3 (51.6 ± 16.3 mL/min) and 12 months (53.6 ± 20.8 mL/min, P = 0.04 versus month 1). Body composition shifted from lean towards fat tissue (25.8 ± 12.5–31.2 ± 11.2% body fat content, P = 0.0001). Only baseline lean weight correlated with fat increase over time (r² = 0.28, P = 0.008). Patients with fat content above median (n = 13) had a 3-fold increased hazard ratio of infection (CI 1.04–9.41, P = 0.042) and overall hospitalization (hazard ratio 2.95, CI 1.10–7.93, P = 0.03). PeakVO₂ decreased over RTx (23.2 ± 6.0– 17.6 ± 5.1 mL/kg/min) and returned to baseline levels not until 1 year later (P < 0.001). After an initial decline, muscle oxidative capacity (peakVO₂/lean mass) improved from 33.6 ± 10.1 to 35.0 ± 8.2 mL/kg/min at 12 months after RTx (P < 0.001).

Conclusions. After RTx, body composition shifted continuously towards fat tissue, and baseline lean weight significantly correlated with fat increase over time. Both severe infections and hospitalizations are associated with a higher fat content before RTx. Exercise capacity (peakVO₂) worsened after RTx and restitutes during follow-up, with muscle quality (peakVO₂/lean) even exceeding baseline levels after 12 months.

Methods. Using data from the United States Renal Data System, we identified individuals initiating dialysis from 1995 to 2004 and categorized their health insurance status. Longitudinal trends in demographic, risk behaviour, functional, comorbidity, laboratory and dialysis modality factors, as reported on the Medical Evidence Form (CMS-2728), were examined in all insurance groups. Polychotomous logistic regression was used to estimate adjusted generalized ratios (AGRs) for these factors by insurance status, with Medicaid as the referent insurance group.

Results. Overall, males constitute a growing percentage of both Medicaid and non-Medicaid patients, but in contrast to other insurance groups, Medicaid has a higher proportion of females. Non-Caucasians also constitute a higher proportion of Medicaid patients than non-Medicaid patients. Body mass index increased in all groups over time, and all groups witnessed a significant decrease in initiation on peritoneal dialysis. Polychotomous regression showed generally lower AGRs for minorities, risk behaviours and functional status, and higher AGRs for males, employment and self-care dialysis, for non-Medicaid insurance relative to Medicaid.

Conclusions. While many broad parallel trends are evident in both Medicaid and non-Medicaid incident dialysis patients, many important differences between these groups exist. These findings could have important implications for policy planners, providers and payers.

Methods. A total of 75 prevalent haemodialysis patients with autogenous AVF using the BH technique were compared with 70 patients using the rope-ladder technique. The following parameters were registered: haematoma occurrence, redness, swelling, aneurysm formation, the use of sharp or dull needles, miscannulations, and interventions. Needling pain and fear of puncture were assessed using a verbal rating scale (VRS). The duration of the follow-up was 9 months.

Results. Patients in the BH group had more unsuccessful cannulations, compared with the rope-ladder method (P < 0.0001), but the frequency of haematoma (P < 0.0001) and aneurysm formation (P < 0.0001) was less. In addition, intervention such as angioplasty (P < 0.0001) was higher in patients using the rope-ladder technique. A negative outcome of the BH technique was the higher incidence of access infections compared to the rope-ladder method.

Conclusion. This study showed that the BH method is a valuable technique with few complications like haematoma, aneurysm formation and the need for interventions. However, the infections induced by the BH method should not be underestimated. This underlines the importance of an aseptic and correct technique of the buttonhole procedure.

Methods. Eighty non-diabetic men with stable angina were followed up for 2 years after elective coronary angioplasty. Exclusion criteria included heart failure, left ventricular systolic dysfunction, eGFR <30 ml/min/1.73 m² and coexistent diseases. Those with cardiovascular events or ejection fraction <55% during the follow-up were also excluded. A baseline blood count of CD34+/kinase-insert domain receptor (KDR)+ cells, a leukocyte subpopulation enriched for EPC, was quantified by flow cytometry (percentage of lymphocytes).

Results. A synergistic interaction (P = 0.015) between decreased CD34+/KDR+ cell counts and increased plasma ADMA, but not symmetrical dimethyl-l-arginine, was the sole significant multivariate eGFR predictor irrespective of baseline eGFR. eGFR was depressed in the simultaneous presence of high ADMA (>0.45 µmol/l, median) and low CD34+/KDR+ cell counts (<0.035%, median) compared to either of the other subgroups (P = 0.001–0.01). eGFR did not correlate with traditional risk factors, angiographic CAD extent, levels of C-reactive protein and soluble vascular cell adhesion molecule-1.

Conclusions. Elevated ADMA and EPC deficiency may synergistically contribute to accelerated renal function decline in stable angina. This could result from the impairment of the EPC-dependent endothelial renewal in the kidney, an NO-dependent process.

Methods. Sixty-seven biopsies, indicated by a rise in creatinine level, were studied. Thirty-four biopsies showing acute T-cell-mediated rejection and 33 displaying inflamed fibrosis were selected. Tregs frequency was calculated for each infiltrate by counting FOXP3+ and CD3+ cells on two contiguous serial sections.

Results. A total of 121 infiltrates were scored with a mean of 309 CD3+ cells per infiltrate (range: 50–700). Tregs were enriched within allografts exhibiting inflamed fibrosis versus acute cellular rejection (10.6 ± 6.8% versus 5.5 ± 2.6%, respectively, P = 0.005). In those with inflammation within scarred areas, the subset of patients with a low FOXP3/CD3 ratio (below the median value) displayed a lower frequency of B-cell-enriched nodular cell clusters (20% versus 86%, P = 0.001) and had a significantly lower graft survival (log-rank, P = 0.02). In multivariate analysis, the low FOXP3/CD3 ratio remained an independent indicator of outcome (P = 0.03). Consistently, the FOXP3+/IL-17+ cell ratio was higher in nodular than in diffuse infiltrates.

Conclusions. Our results suggest that Tregs may dampen the graft injury in chronic (versus acute) inflammation and stress the importance of devising strategies to enhance Tregs efficiency.

Methods. An initial questionnaire survey was undertaken and a 12-month prospective audit performed of renal biopsies against agreed standards for the number of needle passes, adequacy of biopsy material and complication rates.

Results. Eleven of 13 centres participated. Information leaflets are sent pre-biopsy in five centres with only one using play preparation. Six of 11 routinely perform biopsies as day-case (DC) procedures and 6 use general anaesthesia (GA). Real-time ultrasound is the favoured method in eight centres. Biopsies are performed by nephrologists only in four centres, nephrologists with radiologists in five and radiology alone in two. Of 531 biopsies (352 native), 31% were performed as a DC with 49% being done under GA.

 The standard for the number of passes of native kidneys (≤3 in 80%) was achieved in 86.4%, but the standard of ≤2 passes in 80% was achieved in only 73.4% of transplanted kidneys. Adequate tissue was obtained for diagnosis in 97.5% (standard >95%). The major complication rate was higher than the standard of ≤5% at 10.4%. There was no significant difference in complication rates when the biopsy was performed as a DC or inpatient procedure (P = 0.73) or when GA or sedation was used (P = 0.8).

Conclusions. The audit highlights significant variation in clinical practice with limited use of preparation materials and DC procedures. The results have stimulated constructive debate about preparation and indications for biopsy and training issues. The audit enables centres and individuals to monitor performance.

Methods. This study included 4128 subjects from the Cardiovascular Health Study. Cystatin C was measured at baseline, 3 years later and 7 years later; eligible subjects had at least two measures. Cystatin C-based estimated glomerular filtration rate (eGFR_cysC) was estimated, and rapid kidney function decline was defined as an annual loss of eGFR_cysC >3 mL/min/1.73 m². Predictors included ten inflammatory and procoagulant biomarkers: C-reactive protein, interleukin-6, intercellular adhesion molecule-1, white blood cell count, fibrinogen, factor VII, factor VIII, D-dimer, plasmin-antiplasmin complex and serum albumin.

Results. During the study, 1059 subjects (26%) had a rapid decline in kidney function. In contrast to the other nine inflammatory or procoagulant biomarkers, serum albumin had a consistent and inverse association with rapid kidney function decline [final adjusted logistic regression model: 1.14-fold increased odds (95% CI 1.06–1.23) of rapid decline per standard deviation lower albumin]. The lowest quartile of albumin had an odds ratio of 1.55 (95% CI 1.23–1.96) for rapid decline compared with the highest quartile. These associations persisted after adjusting the albumin models for CRP, IL-6 and fibrinogen.

Conclusions. In contrast to nine other inflammatory and procoagulant markers, only lower baseline levels of serum albumin were consistently associated with a rapid decline in kidney function, as measured by cystatin C-based eGFR.

Methods. A population-based nested case-control study was performed in the Swedish organ transplantation cohort (n = 5931). All patients who developed CSCC during the follow-up (1970–97) were eligible as cases (n = 207). Controls (n = 189) were randomly selected from the cohort and individually matched to the cases on follow-up time, age at and calendar period of transplantation. Exposure information was collected through extensive and standardized review of medical records.

Results. The median time to CSCC was 6.7 years. Post-transplant azathioprine (Aza) treatment considerably increased the risk of CSCC during all time periods analysed, and the risk augmented with increasing dose and duration. Patients who after the entire follow-up period had received a high accumulated dose of Aza had an 8.8-fold increased risk of CSCC in multivariate analysis (P < 0.0001), compared to patients never treated with Aza. Additionally, a high accumulated dose of corticosteroids during the same period conferred a 3.9-fold elevated risk of CSCC (P = 0.09), compared to the lowest accumulated dose of corticosteroids. Cyclosporine treatment was not associated with the risk of CSCC post-transplantation.

Conclusions. This study provides evidence that Aza treatment, but not cyclosporine treatment, is strongly associated with post-transplant CSCC risk. The results suggest that the risk of CSCC after organ transplantation is not only an effect of the immunosuppressive load per se.

Methods. In a retrospective cohort of 20 366 adult Medicare primary renal transplant recipients in the USRDS database transplanted from 1 January 2003 to 31 July 2005 and followed through 31 December 2005, we assessed Medicare claims for RM and dyslipidaemia (HPL), which was used as a surrogate for statin use.

Results. The incidence rate of RM post-transplant for the study period was 1.4 (95% CI 1.1–1.8) per 1000 person-years. By Cox regression analysis, cyclosporine (versus tacrolimus) use [AHR 2.36 (95% CI 1.23–4.35); P = 0.006] and black race [AHR 2.33 (95% CI 1.30–4.17); P = 0.005] were associated with RM. By Cox non-proportional hazards regression, RM was associated with graft loss (including death) [AHR 2.84 (95% CI 1.70–4.72); P < 0.001].

Conclusions. RM is a rare complication after renal transplantation and is significantly associated with allograft loss (including death). RM is significantly more likely to occur with cyclosporine (versus tacrolimus)-based immunosuppression and possibly in persons of black race. Increased surveillance for RM is warranted in these at-risk patients.

Methods. A 37-item questionnaire was administered along with the Kidney Disease Quality of Life instrument to 92 patients with CKD not on dialysis (24% black, 5% women, mean age 68 years, 68% with diabetes mellitus). To discover groups of symptoms, agglomerative cluster analysis followed by exploratory common factor analysis was performed. Construct validity, internal reliability, convergent and discriminant validity, test–retest reliability and finally the association of various symptom domains with objective measurements such as estimated GFR and haemoglobin were tested.

Results. The top five symptoms of at least moderate severity in decreasing order of prevalence were ‘tire easily’, limited physical activity, nocturia, joint pain and ‘stop and rest often’. Four common factors emerged that could be broadly classified into neuropsychiatric, cardiovascular, uraemia and anaemia symptoms accounting for 73% of the total variance in the sample. The coefficient alpha for each of these factors approached 0.9. The test–retest reliability in 41 patients over 8 weeks was likewise high. There was good convergent and divergent validity. However, there was little relationship between estimated GFR and symptom scores.

Conclusions. The assessment of symptom burden among patients with CKD may be facilitated by incorporating this instrument in routine practice and clinical trials.

Methods. We simultaneously investigated the temporal changes of nephrocalcinosis-associated parameters during and shortly after a 4-day ethylene glycol (EG)-administration period in rats. We measured oxaluria, crystal formation, crystalluria, apoptosis, epithelial injury/ regeneration and luminal membrane expression of several crystal-binding molecules [hyaluronan (HA), osteopontin (OPN) and for the first time in vivo, annexin-2 (ANX2) and nucleolin-related-protein (NRP) and one of their receptors (CD44, HA/OPN-receptor]. Clinically, renal biopsies of preterm infants, transplant patients and acute phosphate nephropathy patients were stained for ANX2, NRP, HA and OPN.

Results. In the presence of a rather constant and persistent intratubular crystal formation, crystal retention gradually increased during EG-administration and markedly increased after arrest thereof, indicating that the development of crystal adhesion requires more than just the presence of crystals in the tubular fluid. All luminal membrane markers and a regenerating/dedifferentiated epithelium, unlike apoptosis, to various extents were upregulated concurrently and in association with crystal adhesion. However, both in humans and rats, expression of luminal molecules was not confined to crystal-containing tubules.

Conclusions. Altogether, these findings allow better insight into the mechanisms underlying the ‘fixed particle’ theory in vivo and indicate that an altered epithelial phenotype with crystal-binding properties precedes crystal adhesion, thereby corroborating the requirement of tubular epithelial phenotypical changes in the development of intratubular nephrocalcinosis.

Methods. We investigated the structural and functional consequences of acute peritonitis induced by LPS in wild-type (WT) mice versus knockout mice (KO) for the endothelial NOS (eNOS), the inducible NOS (iNOS) or the neuronal NOS (nNOS).

Results. The level of NO metabolites (NOx) in the dialysate was maximal 18 h after LPS injection. LPS induced a significant increase in the transport of small solutes and decreased ultrafiltration in WT mice. These changes, which occurred without vascular proliferation, were paralleled by the upregulation of nNOS and eNOS, and the induction of iNOS. The transport modifications induced by LPS were significantly reversed in eNOS KO mice, but not modified in mice lacking iNOS or nNOS. In contrast, the increase of dialysate NOx was abolished in iNOS KO mice and significantly reduced in eNOS KO mice, but left unchanged in mice lacking nNOS. Mice lacking iNOS also showed more severe inflammatory changes, and a trend towards increased mortality following LPS.

Conclusion. These data demonstrate specific roles for NOS isoforms in the peritoneal membrane and suggest that selective eNOS inhibition may improve peritoneal transport during acute peritonitis.

Methods. We conducted a retrospective clinicopathologic analysis of 213 patients with lupus nephritis. Twenty-six patients had severe segmental glomerulonephritis (SSGN) and 15 patients had diffuse proliferative glomerulonephritis (DPGN). Patients with pure mesangial lupus nephritis [mesangial glomerulonephritis (MesGN)] (N = 13) were used as histologic controls. The degree of immunologic activity detailed by histologic data including light, fluorescent (IF) and electron microscopy (EM) on kidney biopsies and clinical data from patients with severe lupus nephritis were analysed.

Results. Biopsies from patients with SSGN had fewer glomeruli with wire loops (3 ± 6% versus 35 ± 34% P = 0.005) and hyaline thrombi (0.8 ± 3% versus 16 ± 22%, P = 0.02) compared to DPGN. The amount of IgG by IF was less in SSGN lesions compared to DPGN lesions, and IgG was absent in 30% of the SSGN group compared to none of the DPGN group (P = 0.04). There was no difference in mesangial deposits among the three groups (SSGN, DPGN and MesGN). The EM data supported the IF data. Anti-neutrophil cytoplasmic antibodies (ANCA) were essentially negative in all three groups and the C3 values tended to be lower in DPGN compared to SSGN (48 ± 15 mg/dl versus 60 ± 26 mg/dl, P = 0.09).

Conclusions. The findings in DPGN involve a classic immune complex-mediated glomerulonephritis as demonstrated by the abundant immune aggregates witnessed in the peripheral capillary wall. In contrast, a paucity of peripheral immune aggregates is seen in SSGN implying a different pathogenesis. Our data support a mechanism of glomerular injury in SSGN that is separate from the generally accepted unitary concept of immune complex deposition in lupus nephritis.

Methods. We prospectively performed IB-IVUS before elective PCI in 89 consecutive patients with stable angina. According to estimated glomerular filtration rate (eGFR), they were divided into two groups (eGFR <60 ml/min/ 1.73 m² or eGFR ≥60 ml/min/1.73 m²). The tissue characteristics of the coronary plaque at each target stenotic site were evaluated by three-dimensional (3D) IB-IVUS just before PCI procedure.

Results. The patients with eGFR <60 ml/min/1.73 m² had higher percentage of lipid volume and lower percentage of fibrous volume compared to the patients with eGFR ≥ 60 ml/min/1.73 m² on the 3D IB-IVUS images (36.7 ± 10.6% versus 28.7 ± 9.3%, P < 0.001 and 59.1 ± 8.7% versus 66.3 ± 8.3%, P < 0.001, respectively). eGFR showed a significant negative correlation with lipid volume and had a significant positive correlation with fibrous volume in coronary plaques (r = –0.44, P < 0.0001, and r = 0.46, P < 0.0001, respectively).

Conclusions. Impaired renal function was related to higher percentage of lipid volume and lower percentage of fibrous volume in coronary plaque. Our findings may explain the increasing risk of cardiovascular events in patients with renal dysfunction.

Methods. Clinical and renal histopathological data of patients with lupus nephritis were reviewed for clinical and pathological evidence of both TTP–HUS and renal thrombotic microangiopathy (TMA). Serum ADAMTS-13 activity and ADAMTS-13 autoantibodies were further studied.

Results. Seven patients with evidence of both TTP–HUS and renal TMA were identified in 353 patients with lupus nephritis. In comparison with 55 patients with lupus nephritis without TTP–HUS, those with TTP–HUS had a higher prevalence of acute renal failure and worse renal outcome. The serum ADAMTS-13 activity was significantly lower in patients with both lupus nephritis and TTP–HUS than in patients with lupus nephritis only and in normal control (40% versus 69%, P = 0.012; 40% versus 81%, P < 0.001, respectively). The prevalence of ADAMTS-13 autoantibodies was significantly higher in patients with both lupus nephritis and TTP–HUS than in patients with lupus nephritis only and in normal control (6/7, 86% versus 10/55, 18%, P < 0.001; 6/7, 86% versus 0, P < 0.001, respectively). After clinical remission, the serum ADAMTS-13 activity of the seven patients with TTP–HUS increased significantly (40% versus 63%, P < 0.001) and five out of the six patients with positive ADAMTS-13 autoantibodies turned negative.

Conclusions. ADAMTS-13 autoantibodies might play an important role in the pathogenesis of TTP–HUS associated with lupus nephritis. The long-term outcome seems to be worse in patients with both TTP–HUS and lupus nephritis than in patients with lupus nephritis alone.

Methods. This is a symptomatic review and meta-analysis of prospectively randomized studies, abstracts and manuscripts, published from 1950 to 20 February 2009.

Results. Of 192 identified publications, 18 studies (n = 3055) were included. Nine studies were only published as an abstract. CI-AKI occurred in 11.6%. Six prospective studies demonstrated that intervention with sodium bicarbonate resulted in a decreased risk of CI-AKI. The aggregate result of the prospective trials also demonstrated a benefit favouring sodium bicarbonate (RR = 0.66, 95% CI = 0.45–0.95). This effect was most prominent in coronary procedures and in patients with chronic kidney disease. There was no effect on need for renal replacement therapy (RRT) and mortality. Published manuscripts demonstrated a beneficial effect, while abstracts could not. Also, funnel plot analysis suggested a publication bias. In addition, we found significant clinical and statistical heterogeneity between studies. Finally, the quality of the individual studies was limited.

Conclusions. The incidence of CI-AKI was higher than recently reported, and varied among study cohorts. We found a preventive effect of the use of sodium bicarbonate on the risk for CI-AKI, however, with borderline statistical significance. There was no effect on need for RRT or mortality. The relative low quality of the individual studies, heterogeneity and possible publication bias means that only a limited recommendation can be made in favour of the use of sodium bicarbonate.

Methods. A total of 44 HD patients were followed for 6 months. BC was assessed by multifrequency bioimpedance (BIA). Serum concentrations of cardiac troponin T (cTnT), high-sensitive C-reactive protein (hsCRP), brain natriuretic peptide (BNP) and N-terminal proBNP (NT-proBNP) were assessed at 2 monthly intervals. The longitudinal data analysis was conducted with a marginal model.

Results. During the follow-up, the parameters describing the BC were highly predictive of both BNP and NT-proBNP and independent of gender, time, hsCRP and cTnT concentrations. The intracellular water (ICW)/body weight (BW) ratio (reflecting malnutrition) exerted a negative effect, whereas the extracellular water (ECW)/BW ratio (reflecting overhydration) had a positive effect on BNP and NT-proBNP concentrations. HsCRP and cTnT concentrations were significantly associated with each other. Furthermore, NT-proBNP concentrations were predictive of cTnT and hsCRP concentrations.

Conclusions. In the present study, we find a significant relation between BIA-derived BC parameters and natriuretic peptide concentrations. This relationship was independent of the cardiac history of the patient and suggests that the natriuretic peptide levels are to some degree modifiable by changing a patient's fluid distribution. Moreover, cTnT, BNP, NT-proBNP and hsCRP were significantly related, showing a complex relation between overhydration, malnutrition, inflammation and cardiac biomarkers in dialysis patients.

Methods. We performed a single centre, non-randomized, open-label phase I/II study in maintenance HD patients with a 4-week, escalating dose regimen of oligofructose-enriched inulin (ORAFTI®Synergy 1, Tienen, Belgium) (www.clinicaltrials.gov NCT00695513). Changes in p-cresyl sulfate and indoxyl sulfate serum concentrations as well as changes in p-cresyl sulfate and indoxyl sulfate generation rates were analysed.

Results. Compliance with therapy was excellent. p-Cresyl sulfate serum concentrations at 4 weeks were significantly reduced by 20% (intention to treat, P = 0.01; per protocol, P = 0.03). Also p-cresyl sulfate generation rates were reduced (P = 0.007). In contrast, neither indoxyl sulfate generation rates (P = 0.9) nor serum concentrations (P = 0.4) were significantly changed.

Conclusion. The prebiotic oligofructose-inulin significantly reduced p-cresyl sulfate generation rates and serum concentrations in haemodialysis patients. Whether reduction of p-cresyl sulfate serum concentrations, an independent predictor of cardiovascular disease in HD patients, will result in improved cardiovascular outcomes remains to be proven.

Methods. Innate B1 cells (CD19+, CD5+), conventional B2 cells (CD19+, CD5–), newly formed transitional B cells (CD19+, CD10+, CD27–), naïve B cells (CD19+, CD27–) and memory B cells (CD19+, CD27+) and BAFF receptor were quantified by flow cytometry. Plasma IL-7, BAFF, IL-6, TNF- and IL-10 were measured by ELISA.

Results. The ESRD group exhibited significant reductions of all B-cell subpopulations except for transitional B cells that were less severely affected. No significant difference was found in B-cell apoptosis between the ESRD and control groups. Moreover, plasma IL-7 and BAFF levels were elevated in ESRD patients, therefore excluding their deficiencies as a possible culprit. However, BAFF receptor expression was significantly reduced in transitional but not mature B cells in the ESRD group. Interestingly, B-cell activation with the TLR9 agonist resulted in significantly greater production of IL-6 and TNF alpha but not IL-10 in the ESRD group.

Conclusions. Thus, despite elevation of B-cell growth, differentiation and survival factors, ESRD patients exhibited diffuse reduction of B-cell subpopulations. This was associated with the down-regulation of BAFF receptor in transitional B cells. The latter can, in part, contribute to B-cell lymphopenia by promoting resistance to the biological actions of BAFF that is a potent B-cell differentiation and survival factor.

Methods. Recruited studies met the following criteria: they were randomized controlled trials or historical cohort studies; subjects consisted of adults (age, ≥ 18 years) undergoing PD; mupirocin treatment was administered to the therapy group and placebo or no treatment was administered to the control group. The primary extracted data were the difference in the episodes of ESI and peritonitis S. aureus or other organisms among treatment and control groups.

Results. Fourteen studies described in 13 articles and a total of 1233 patients versus 1217 controls were included in the analysis. Of the 13 articles, 6 were newly published articles that had not been analysed previously and 3 were randomized controlled trials. The application of mupirocin decreased the risk by 72% [95% confidence interval (CI): 0.60–0.81] in ESI and by 70% (95% CI 0.52–0.81) in peritonitis due to S. aureus among all patients undergoing PD. Treatment of mupirocin reduced the risks of ESI and peritonitis due to all organisms by 57% (95% CI: 0.46–0.66) and 41% (95% CI: 0.24–0.54), respectively. Based on the six newly published articles, the reduced risk rate for mupirocin therapy was found to be 80% (95% CI: 0.39–0.93, P = 0.004) in ESI and 91% (95% CI: 0.72–0.97, P < 0.0001) in peritonitis due to S. aureus; 70% (95% CI: 0.47–0.82, P < 0.0001) in ESI and 42% (95% CI: 0.25–0.55, P < 0.0001) in peritonitis due to all organisms among mupirocin-treated and -untreated subjects. Based on the three randomized controlled trials, ESI and peritonitis due to S. aureus were found to be reduced by 73% (95% CI: 0.63–0.80, P < 0.0001) and 40% (95% CI: 0.17–0.56, P = 0.002), respectively. Interestingly, although mupirocin treatment can reduce the risk rate of ESI by 46% (95% CI: 0.35–0.55, P < 0.00001), it cannot decrease the risk rate of peritonitis due to all organisms (P = 0.56).

Conclusions. Mupirocin prophylaxis was effective on preventing ESI and peritonitis due to S. aureus and other organisms in PD patients.

Methods. We analysed data from a multicentre observational study of acute kidney injury in critically ill patients. We identified 12 non-dialysed, non-oliguric patients with consecutive increases in creatinine for at least 3 and up to 7 days who had measurements of urinary creatinine clearance. Glomerular filtration rate was estimated by Cockcroft–Gault, Modification of Diet in Renal Disease, Jelliffe equation and Jelliffe equation with creatinine adjusted for fluid balance (Modified Jelliffe) and compared to measured urinary creatinine clearance.

Results. Glomerular filtration rate estimated by Jelliffe and Modification of Diet in Renal Disease equation correlated best with urinary creatinine clearances. Estimated glomerular filtration rate by Cockcroft–Gault, Modification of Diet in Renal Disease and Jelliffe overestimated urinary creatinine clearance was 80%, 33%, 10%, respectively, and Modified Jelliffe underestimated GFR by 2%.

Conclusion. In patients with acute kidney injury, glomerular filtration rate estimating equations can be improved by incorporating data on creatinine generation and fluid balance. A better assessment of glomerular filtration rate in acute kidney injury could improve evaluation and management and guide interventions.

Methods. Glomerular filtration rate (eGFR) was calculated in consecutive patients referred for full-night observed in-hospital polysomnography. SA was defined as the respiratory disturbance index (RDI) > 5.

Results. One hundred and fifty-eight patients were studied. The age (mean ± SD) was 61.2 ± 12.7 years, body mass index 29.5 ± 5.9 kg/m² and eGFR 86.1 ± 21.7 mL/min/1.73 m². SA was present in 133 patients (85%). The eGFR was 94.6 7 mL/min/1.73 m² in patients without SA and 84.5 7 mL/min/1.73 m² in patients with SA [mean difference (95% confidence interval) 10.0 (0.6–19.4) mL/min/1.73 m²; P = 0.037]. Seventy patients had eGFR ≥ 90 mL/min/1.73 m² (group 1), and 70 patients had between 60 and 89 mL/min/1.73 m² (group 2), and 18 patients had 30–59 mL/min/1.73 m² (CKD 3). Although the prevalence of SA did not differ among the groups (group 1: 80%; group 2: 86%; CKD 3: 94%), the number of central sleep apnoeas (CSA) per hour was 5.9 ± 12.2 in CKD 3, six times greater compared to patients with eGFR ≥ 60 mL/min/1.73 m² (1.0 ± 2.1; P = 0.01). The prevalence of obstructive SA did not differ between the groups. After adjustment for age, gender, BMI, hypertension, diabetes mellitus and smoking status, CKD 3 (P = 0.0004) and New York Heart Association class ≥3 (P = 0.0001) remained predictive of CSA events per hour.

Conclusions. eGFR is reduced in patients with SA, particularly in those with episodes of CSA.

Methods. A prospective multicentre cohort of 753 prevalent adult patients on CAPD, APD and HD was followed up for 16 months. Plasmatic levels of NT-proBNP, extracellular fluid volume/total body water ratio (ECFv/TBW) and traditional clinical and biochemical markers for cardiovascular damage risk were measured, and their role as predictors of all-cause and cardiovascular mortality was analysed.

Results. NT-proBNP level, ECFv/TBW and other cardiovascular damage risk factors were not evenly distributed among the different dialysis modalities. NT-proBNP levels and ECFv/TBW were correlated with several inflammation, malnutrition and myocardial damage markers. Multivariate analysis showed that NT-proBNP levels and ECFv/TBW were predictors of both all-cause and cardiovascular mortality, independently of dialysis modality and the presence of other known clinical and biochemical risk factors.

Conclusions. NT-proBNP is a reliable predictor of death risk independently of the effect of dialysis modality on fluid volume control, and the presence of other clinical and biochemical markers recognized as risk factors for all-cause and cardiovascular mortality. NT-pro-BNP is a good predictor of mortality independently of fluid volume overload and dialysis modality.

Methods. Four Italian dialysis centres enrolled 355 PD patients with 2916 fluid collections. To rank the equations, their accuracy (median absolute percentage error, MAPE), precision (root mean square error, RMSE), agreement (k statistics), sensitivity and specificity (area under ROC curves, AUC, where x = 1 – specificity and y = sensitivity) were calculated with reference to the measured totCrCL.

Results. The Gates, Virga and 4-MDRD equations showed the best global performance as concerns accuracy (MAPE = 14.1, 16.3, 15.9% respectively), precision (RMSE = 13.2, 13.3, 13.4), agreement (k = 0.425, 0.440, 0.375), sensitivity and specificity (AUC = 0.825, 0.826, 0.820), while the Cockcroft–Gault formula revealed a rather poor reliability.

Conclusions. Fluid collection remains the gold standard for assessing PD adequacy. Our study ascertained how 12 Cr-based equations performed in estimating totCrCL in PD patients with a view to enabling the most accurate and precise among them to be chosen for use in approximately assessing totCrCL.

Methods. We conducted a retrospective cohort study to investigate the relationship between CKD and serum phosphorous. Through clinical databases at a large health maintenance organization, we identified a dynamic CKD inception cohort between 1997 and 2004, with stage 3–5 kidney disease with subsequent phosphorous measurement; the patients were followed up for up to 5 years for outcomes of mortality, cardiovascular mortality, cardiovascular hospitalizations and renal replacement therapy (RRT; dialysis or transplant). Survival analysis with time-varying covariables for phosphorous and renal function estimated the relationship between phosphorous level and outcomes, adjusting for potential confounding variables.

Results. A total of 930 patients with complete data were included in our analysis; they had a higher disease burden than excluded patients. Phosphorous did not predict overall or cardiovascular mortality, or cardiovascular hospitalizations. The rate of RRT increased significantly with the level of phosphorous, even when controlling for renal function.

Conclusions. Contrary to some previous reports, we did not find evidence of increased mortality with phosphorous, but did find that increased levels of phosphorous are related to excess rates of RRT. Our work does not suggest that controlling phosphorous will lower the risk of RRT; our work motivates randomized controlled trials to investigate the clinical value of such interventions.

Methods. Because of the contradictory reports concerning rapamycin on proteinuria, we examined proteinuria and podocyte damage markers on two renal disease models, with clearly different pathophysiological mechanisms: a glomerular toxico-immunological model induced by puromycin aminonucleoside, and a chronic hyperfiltration and inflammatory model by mass reduction, both treated with a fixed high rapamycin dose.

Results. In puromycin groups, rapamycin provoked significant increases in proteinuria, together with a significant fall in podocin immunofluorescence, as well as clear additional damage to podocyte foot processes. Conversely, after mass reduction, rapamycin produced lower levels of proteinuria and amelioration of inflammatory and pro-fibrotic damage. In contrast to the puromycin model, higher glomerular podocin and nephrin expression and amelioration of glomerular ultrastructural damage were found.

Conclusions. We conclude that rapamycin has dual opposing effects on subjacent renal lesion, with proteinuria and podocyte damage aggravation in the glomerular model and a nephro-protective effect in the chronic inflammatory tubulointerstitial model. Rapamycin produces slight alterations in podocyte structure when acting on healthy podocytes, but it clearly worsens those podocytes damaged by other concomitant injury.

Methods. Mouse cortical collecting duct (mpkCCD) cells were incubated with ANP, l-arginine and 8-Br-cGMP for 2 h and subjected to immunocytochemistry and cell surface biotinylation assays to examine their effect on AQP2 translocation. To test the effect of cGMP pathway activators on AQP2 expression, the mpkCCD cells were treated with dDAVP, ANP and l-arginine for 4 days, or with 8-Br-cGMP for the last day. AQP2 protein levels were determined by immunoblotting.

Results. ANP, l-arginine and 8-Br-cGMP induced the translocation of AQP2 in the mpkCCD cells. However, in contrast to dDAVP, ANP, l-arginine and 8-Br-cGMP did not increase the expression of AQP2.

Conclusions. Our results suggest that while activators of the cGMP pathway are likely beneficial in the treatment of X-linked NDI, their ability to relieve NDI in the patients may be improved when combined with agents stimulating AQP2 expression.

Methods. This study enrolled 29 intra-dialytic hypotensive patients (the IDH group) and 34 controls (the CON group) on regular maintenance haemodialysis. The RT3DE- and 2D-derived ejection fraction (EF), stroke volume index (SVI) and ratio of early transmitral inflow velocity to diastolic early tissue velocity were assessed at pre-dialysis and mid-dialysis. The intravascular volume was assessed by the inferior vena cava collapsibility index.

Results. Pre-dialysis evaluation showed no difference in RT3DE- and 2D-derived parameters between the two groups. At mid-dialysis, the IDH group had a lower 2D EF (54 ± 9.1 versus 62 ± 6.8% in the CON group, P < 0.001), RT3DE EF (53 ± 6 versus 60 ± 7% in the CON group, P < 0.001) and SVI (24.3 ± 8 versus 30.6 ± 12.2 mL in the CON group, P = 0.02). From pre-dialysis to mid-dialysis, the IDH group had greater decrease in the change in 2D EF (–4.8% ± 12.6% versus 5% ± 13.7% in the CON group, P = 0.004), RT3DE EF (–11.8 ± 10.3 versus –3.4 ± 11.5% in the CON group, P = 0.003) and SVI (–17.3 ± 18.5 versus –9.2 ± 19.8% in the CON group, P = 0.004). The calculated cardiac index change also showed a greater decrease in the IDH group (–17.8 ± 20.2 versus –5.7 ± 18.5% in the CON group, P = 0.02). No significant difference in the ratio of early transmitral inflow velocity to diastolic early tissue velocity, heart rate, systemic vascular resistance index or inferior vena cava collapsibility index was found between the two groups at the baseline or mid-dialysis. A lack of an increase in heart rate and the systemic vascular resistance index in the IDH group during the hypotensive episodes implies that these patients have autonomic dysfunction. Multivariate analysis showed that the RT3DE EF change of < –9.5% (odds ratio = 6, P = 0.003) and the presence of diabetes (odds ratio = 4.4, P = 0.013) had significant and independent associations with intra-dialytic hypotension.

Conclusions. By adopting RT3DE to assess LV performance, our data demonstrated that an inadequate compensation in the LV systolic function is the main mechanism mediating the occurrence of intra-dialytic hypotension in patients with autonomic dysfunction.

Methods. We conducted a randomized open-label study in patients with iMN, a normal renal function and a high risk for ESRD (urinary β2m >0.5 µg/min, UIgG >125 mg/ day). Patients started with immunosuppressive therapy (cyclophosphamide for 12 months, and steroids) either immediately after randomization or when renal function deteriorated (sCr ≥+25% and sCr >135 µmol/l or sCr ≥+50%). End points were remission rates, duration of the nephrotic syndrome (NS), renal function and complications.

Results. The study included 26 patients (24 M/2 F), age 48 ± 12 years; sCr 96 µmol/l (range 68–126) and median proteinuria 10.0 g/10 mmol Cr. Early treatment resulted in a more rapid onset of remission (P = 0.003) and a shorter duration of the NS (P = 0.009). However, at the end of the follow-up (72 ± 22 m), there were no differences in overall remission rate, sCr (93 versus 105 µmol/l), proteinuria, relapse rate and adverse events.

Conclusions. In high-risk patients with iMN, immunosuppressive treatment is effective in inducing a remission. Early treatment shortens the duration of the nephrotic phase, but does not result in better preservation of renal function. Our study indicates that treatment decisions must be based on risk and benefit assessment in the individual patient.

Methods. Sprague-Dawley rats were randomized into six groups: (1) sham-op, (2) SNX without treatment, (3) SNX + quinapril (Q), (4) SNX + spironolactone (S), (5) SNX + combination therapy (Q+S), (6) SNX + combination hydrochlorothiazide + reserpin + hydralazine (HRH). Albuminuria and blood pressure were monitored, and kidneys were examined by morphometric and molecular methods.

Results. In SNX rats, albumin excretion was significantly higher than in sham-op rats. Blood pressure reduction was not significantly different between the treatment groups. All therapies (S, Q, Q+S and HRH) reduced albuminuria; the values were lowest in animals treated with Q+S. The volume density of glomerular matrix and the number of mesangial cells were significantly increased in SNX and were lowest in SNX treated with Q+S. The number of podocytes was reduced in SNX, but was normalized in SNX treated with Q+S. Glomerular volumes and podocyte volumes were significantly higher in SNX than in sham-op. Both volumes were reduced by all interventions, but almost normalized by treatment with Q+S. Expression of collagen IV, TGF-β₁ and desmin was increased after SNX and significantly reduced by treatment with Q and Q+S.

Conclusions. In subtotally nephrectomized rats, mineralocorticoid blockade provided additional renoprotection over and above ACE inhibition. Such benefit was paralleled by major changes in podocyte number and morphology and was not blood pressure dependent.

Methods. PTC blood flow was initially monitored using a pencil-lens interval microscope before and after intravenous AII (30 ng/kg/min) infusion with or without azelnidipine (10 µg/kg/min). Next, Wistar rats were treated with chronic infusion of AII (500 ng/kg/min) via an osmotic minipump with or without azelnidipine (3 mg/kg/day, orally) or nifedipine (60 mg/kg/day, orally) for 14 days, and tubulointerstitial damage (PTC loss, interstitial fibrosis, tubular atrophy) was examined.

Results. PTC blood flow was reduced after AII infusion but improved after a bolus injection of azelnidipine. Tubulointerstitial damage observed in chronically AII-treated kidneys was associated with hypoxic conditions, as indicated by the measurement of hypoxia biomarkers (intracellular hypoxyprobe-1 adducts). These tubulointerstitial injuries in AII-infused rats were more effectively reduced by azelnidipine than by nifedipine. The area showing hypoxic conditions in the kidney was also more reduced with azelnidipine than nifedipine treatment.

Conclusions. Azelnidipine may increase PTC blood flow and improve renal hypoxia and tubulointerstitial injury induced by AII infusion.

Methods. Visceral adipose tissue was harvested from normal rats, and adipocytes were isolated and incubated for 2–4 h in media containing 90% plasma from 12 ESRD patients (before and after haemodialysis) and 12 normal control subjects.

Results. The ESRD group had a marked elevation of plasma TNF-, IL-6, IL-8 and leptin concentrations before and after haemodialysis. Incubation in media containing plasma from the ESRD group elicited a much greater leptin release by adipocytes than that containing normal plasma. Post-dialysis plasma evoked an equally intense leptin release. The rise in leptin release was coupled with a parallel fall in TNF- concentration in the incubation media. In contrast to leptin, adiponectin release in the presence of uraemic plasma was similar to that found with the control plasma.

Conclusions. Exposure to uraemic plasma induces exuberant release of leptin that is coupled with avid uptake of TNF- by visceral adipocytes. These observations confirm the role of TNF-, formerly known as cachexin, in the over-production and release of leptin in patients with ESRD.

Methods. The study consisted of 82 Chinese idiopathic FSGS patients (55 patients had nephrotic syndrome: NS) and 90 healthy individuals. Genomic DNA extracted from peripheral leukocytes of patients of healthy individuals were used to analyse the ACTN4 and SYNPO gene promoter mutations by polymerase chain reaction (PCR) and direct sequencing. Mutations were matched with GenBank and TRANSFAC software database (www.genometix.de; www.gene-regulation.com). A dual luciferase assay system was used to analyse the effects of mutations based on PGL3-Basic vector, pRL-SV40 vector, a PC12 cell line and podocytes in vitro. Kidney alpha-actinin-4 and synaptopodin expression of mutated patients and genomic DNA of their parents were investigated.

Results. The study detected the ACTN4 gene promoter 1–34C>T, 1–590delA and (1–1044delT)+(1–797T>C)+(1–769A>G) heterozygous mutations in three patients, respectively, and the SYNPO gene promoter 1–24G>A and 1–851C>T heterozygous mutations in two patients, respectively (with adenine of translation start site ATG naming +1). The same mutations were not found in the control group of 90 healthy people. Excepting one patient with an ACTN4 gene promoter mutation who inherited her parents’ 1–1044delT and 1–797T>C mutated chromosome, respectively, the same mutations were not found in patients’ parents. Alpha-actinin-4 and synaptopodin protein expression are reduced in mutated patients’ kidneys. Dual luciferase assays show that compared to the normal group (with the exception of the 1–1044delT group), luciferase activity in mutated groups decreased for the most part. (1–1044delT)+(1–797T>C)+(1–769A>G) mutations are associated with poor clinical outcomes, and patients with these mutations progress to end-stage renal failure.

Conclusion. The study detected heterozygous mutations in the promoters of the ACTN4 and SYNPO genes in patients with idiopathic FSGS. These mutations affected gene transcription in vitro and may affect protein translation in vivo. So we presumed that the ACTN4 and SYNPO promoter mutations might also contribute to pathophysiology of idiopathic FSGS.

Methods. The prevalence of HF and its effects on all-cause mortality were studied in 163 consecutive patients with systemic hypertension and chronic kidney disease (serum creatinine >2 mg/dL) who underwent percutaneous transluminal renal angioplasty (PTRA) with stenting for atherosclerotic RAS. In addition, in 100 patients with RAS and coexistent HF, we compared the impact of medical treatment (n = 50) versus PTRA (n = 50) on clinical outcomes.

Results. HF (predominantly normal ejection fraction) was present in 50/163 (31%) patients with systemic hypertension and chronic kidney disease (serum creatinine >2 mg/ dL) undergoing PTRA for RAS and represented the major predictor of all-cause mortality in these patients. When compared with sex-matched RAS and HF patients treated medically, PTRA with stenting was associated with a significant decrease in the New York Heart Association Functional Class (1.9 ± 0.8 versus 2.6 ± 1.0, P < 0.04) and a 5-fold reduction in the number of hospitalizations. However, renal artery revascularization did not impact mortality.

Conclusion. HF was present in one-third of patients with renal dysfunction and atherosclerotic RAS who were referred for PTRA. The presence of HF was associated with a significantly increased risk of death after PTRA with stenting. Renal artery revascularization resulted in improved HF control and a reduction in HF hospitalizations.

Methods. CFH autoantibodies were identified and antibody levels were analysed in three aHUS patients during the disease course by the ELISA method. Epitope mapping was performed using recombinant factor H fragments and domain-mapped monoclonal antibodies. The effect of the antibodies on cell-protective activity of CFH was measured by haemolytic assays. CFH:autoantibody complexes were analysed by ELISA.

Results. All three autoantibodies bound to the C-terminal domain of CFH, which is essential for CFH binding to cell surfaces. In patient 1, plasma exchanges and immune adsorption temporarily reduced the autoantibody titre and led to temporary clinical improvement. In patient 2, plasma exchanges and long-term immunosuppression strongly reduced the CFH autoantibody level, and induced a stable remission of aHUS. Patient 3 had lower autoantibody levels that decreased during the follow-up and is in good clinical condition. The patients’ plasma samples caused enhanced lysis of sheep erythrocytes, and the degree of lysis correlated with the CFH autoantibody titre and the amount of CFH:autoantibody complexes. An addition of purified CFH to aHUS plasma or removal of IgG inhibited the haemolytic activity.

Conclusion. These results support a direct role of the autoantibodies in aHUS pathology by inhibiting the regulatory function of CFH at cell surfaces and suggest that reduction of the autoantibody titre is beneficial for the patients.

Methods. CsA was stopped and sirolimus (SRL) commenced immediately and the transfer was covered with prednisolone. Those on azathioprine (AZA) were transferred to MMF. In protocol A, the SRL target concentration was 16 (12–20) ng/ml; in protocol B, the target concentration was 7(5–10) ng/ml, but mycophenolate (MMF) and steroids were commenced prior to the transfer.

Results. Baseline characteristics were similar in both groups except that group B were switched later after transplantation. Renal function improved significantly in both groups; this was maintained up to 1 year. Two patients in group A experienced acute rejection (ISHLT grade 3A or 2R); none was seen in group B. Six patients (46%) remained on protocol A and 22 (85%) remained on protocol B at 1 year.

Conclusions. MMF-SRL substitution resulted in a rapid but partial improvement in renal function; the lower dose SRL regimen was better tolerated.

Methods. Sixteen rats daily received 10 ml of conventional PDF for 4–5 weeks intraperitoneally. Half of them (n = 8) daily received celecoxib (20 mg/kg BW) via oral gavage, and the other half (n = 8) received vehicle via oral gavage. The study also included two control groups (no PDF instillations), each consisting of n = 8 animals that daily received celecoxib or vehicle, respectively, via oral gavage. Functional, morphological and cellular parameters were analysed.

Results. PDF exposure induced an inflammatory condition evidenced by the increased leucocyte number and synthesis of MCP-1, VEGF and hyaluronic acid. After PDF exposure, the omentum showed intense angiogenesis and milky spots formation. Parietal peritoneum showed increased angiogenesis, lymphangiogenesis, submesothelial matrix thickness and enhanced expression of mesothelial aquaporin1 (Aqp1). Concomitant PDF and celecoxib exposure drastically reduced PGE2 levels, angiogenesis, lymphangiogenesis, fibrosis and milky spot formation in studied tissues, but did not modify mesothelial Aqp1 expression nor the tissue expression of VEGF and inflammatory markers. PDF exposure induced severe UF failure that celecoxib treatment completely prevented.

Conclusions. Altogether, celecoxib treatment improves UF capacity and reduces morphological alterations in our rat PD model.

Methods. This was a retrospective study based on the data of the French Language Peritoneal Dialysis Registry (RDPLF). We retrospectively analysed 1613 patients older than 75 years who started PD between January 2000 and December 2005. The end of the observation period was 31 December 2007.

Results. The mean age at dialysis initiation was 81.9 years; 545 patients had a Charlson comorbidity index (CCI) >9. Of these 1613 patients, 1435 were treated by continuous ambulatory peritoneal dialysis (CAPD) and 1232 were on assisted PD. The median patient survival was 27.1 months. In the multivariate analysis, patient survival was associated with sex, age, modified CCI, method of assistance and underlying nephropathy. The median pure technique survival was 21.4 months. In the Cox model, technique survival was associated with the modified CCI, but the association did not remain significant after adjustment for the centre size. The median survival free of peritonitis was 32.1 months. Neither the modality of assistance nor the centre size was associated with peritonitis risk.

Conclusion. PD is a suitable method for elderly patients. In order to increase the rate of PD utilization in elderly patients, the need for the funding of assisted peritoneal dialysis has to be taken into account.

Methods. This was a multi-centre, open-label, randomized, crossover design study. Thirty-one haemodialysis patients were randomly assigned to either sevelamer carbonate powder or sevelamer hydrochloride tablets for 4 weeks followed by a crossover to the other regimen for an additional 4 weeks.

Results. The mean serum phosphorus was 1.6 ± 0.5 mmol/L (5.0 ± 1.5 mg/dL) during sevelamer carbonate powder treatment and 1.7 ± 0.4 mmol/L (5.2 ± 1.1 mg/dL) during sevelamer hydrochloride tablet treatment. Sevelamer carbonate powder and sevelamer hydrochloride tablets are equivalent in controlling serum phosphorus; the geometric least square mean ratio was 0.95 (90% CI 0.87–1.03). No statistically significant or clinically meaningful differences were observed in calcium x phosphorus product and lipid levels between sevelamer carbonate powder and sevelamer hydrochloride tablets. Serum bicarbonate levels increased 2.7 ± 3.7 mmol/L (2.7 ± 3.7 mEq/L) during sevelamer carbonate treatment. No statistically significant change in bicarbonate was observed during sevelamer hydrochloride treatment. Sevelamer carbonate powder and sevelamer hydrochloride were well tolerated during this study.

Conclusions. Sevelamer carbonate powder and sevelamer hydrochloride tablets are equivalent in controlling serum phosphorus and well tolerated in CKD patients on haemodialysis. Bicarbonate levels improved only during sevelamer carbonate treatment. Sevelamer carbonate powder should provide a welcomed new option for the treatment of hyperphosphataemia for CKD patients on dialysis.

Methods. In a prospective fashion, symptoms of depression were evaluated in ESRD patients on RRT using the depression subscore of the Hospital Anxiety and Depression Scale (HADS). Fatal and non-fatal clinical events were determined during a 1-year follow-up.

Results. Of 101 patients with ESRD, 42% showed manifest depressive symptoms, defined as a HADS-D score ≥7. No association was found between depressive symptoms and severity of somatic disease. During follow-up, all-cause mortality was significantly higher in patients with depressive symptoms above threshold (n = 42, mortality: 26%) compared to patients with depressive symptoms below threshold (n = 59, mortality 8%), (crude HR 3.3, CI 1.2–9.6, P = 0.02). The excess in mortality was mainly caused by a higher incidence of septicaemia (0 versus 12%, P = 0.01). After adjustment for clinical parameters, this association between depressive symptoms and mortality became even stronger. There was no significant difference observed in the incidence of cardiovascular events.

Conclusions. Patients with ESRD treated with dialysis show a high level of depressive symptoms that is independently associated with poor survival. Future research should address appropriate therapeutic regimens.

Methods. Plasma H₂S levels were measured with a common spectrophotometric method. This method detects various forms of H₂S, protein-bound and non-protein-bound. Blood sulphaemoglobin, a marker of chronic exposure to H₂S, was also measured, as well as related sulphur amino acids, vitamins and transcriptional levels of relevant genes, in haemodialysis patients and compared to healthy controls.

Results. Applying the above-mentioned methodology, H₂S levels were found to be decreased in patients. Sulphaemoglobin levels were significantly lower as well. Plasma homocysteine and cysteine were significantly higher; vitamin B₆, a cofactor in H₂S biosynthesis, was not different. H₂S correlated negatively with cysteine levels. CSE expression was significantly downregulated in haemodialysis patients.

Conclusions. Transcriptional deregulation of genes encoding for H₂S-producing enzymes is present in uraemia. Although the specificity of the method employed for H₂S detection is low, the finding that H₂S is decreased is complemented by the lower sulphhaemoglobin levels. Potential implications of this study relate to the pathogenesis of the uraemic syndrome manifestations, such as hypertension and atherosclerosis.

Methods. One hundred and seven patients (60.4 ± 14.6 years) with CKD (mean glomerular filtration rate = 34 ± 17 mL/min/1.73 m²) were included in this cross-sectional study. Common carotid artery diameter, intima–media thickness and carotid stiffness were determined with an echotracking system. Bone evaluation was performed by bone densitometry and the measurement of a bone-remodeling marker, bone-specific alkaline phosphatase (BSALP).

Results. After adjustment for age, sex, mean blood pressure, carotid pulse pressure and glomerular filtration rate, bone mineral densities measured at the radius, hip and lumbar spine were significantly and negatively correlated with carotid internal diameter (P = 0.0001, P = 0.0003, P = 0.01, respectively). This association exists only in patients with glomerular filtration rate ≤38 mL/min/ 1.73 m². BSALP was independently and positively correlated with carotid internal diameter and explained 13% of the variance.

Conclusions. Bone mineral density and serum marker of bone remodeling are independently correlated with arterial remodeling in CKD patients suggesting a crosstalk between kidney, arterial wall and bone.

Method. A randomized Latin square cross-over study was used to evaluate the three different concentrations of D_Ca (1.00, 1.25 and 1.50 mmol/L) during the second HD of the week for 3 consecutive weeks. Subjects returned to their baseline D_Ca for the following two treatments, allowing for a 7-day washout period between each experimental HD. cPWP, carotido-radial (c-r) and carotido-femoral (c-f) pulse wave velocities (PWV), plasma level of ionized calcium (iCa) and intact parathyroid hormone (PTH) were measured prior to and immediately after each experimental HD session. Data were analysed by the general linear model for repeated measures and by the general linear mixed model.

Results. Eighteen patients with a mean age of 48.9 ± 18 years and a median duration of HD of 8.7 months (range 1–87 months) completed the study. In post-HD, iCa decreased with D_Ca of 1.00 mmol/L (–0.14 ± 0.04 mmol/L, P < 0.001), increased with a D_Ca of 1.50 mmol/L (0.10 ± 0.06 mmol/L, P < 0.001) but did not change with a D_Ca of 1.25 mmol/L. Tests of within-subject contrast showed a linear relationship between higher D_Ca and a higher post-HD c-f PWV, c-r PWV and mean BP (P < 0.001, P = 0.008 and P = 0.002, respectively). Heart rate-adjusted central augmentation index (AIx) decreased significantly after HD, but was not related to D_Ca. The timing of wave refection (Tr) occurred earlier after dialysis resulting in a linear relationship between higher D_Ca and post-HD earlier Tr (P < 0.044). In a multivariate linear-mixed model for repeated measures, the percentage increase in c-f PWV and c-r PWV was significantly associated with the increasing level of iCa, whereas the increasing level of MBP was not significant. In contrast, the percentage decrease in Tr (earlier wave reflection) was determined by higher MBP and higher ultrafiltration, whereas the relative change in AIx was inversely determined by the variation in the heart rate and directly by MBP.

Conclusion. We conclude that D_ca and acute changes in the serum iCa concentration, even within physiological range, are associated with detectable changes of arterial stiffness and cPWP. Long-term studies are necessary to evaluate the long-term effects of D_Ca modulation on arterial stiffness.

Methods. A total of 48 patients with anti-GBM disease and 225 geographically and ethnically matched healthy controls were involved. Genotyping of the previously identified polymorphisms FCGR2A131H/R (rs1801274), FCGR2B 232I/T (rs1050501) and FCGR3A176F/V (rs396991) were detected by the TaqMan genotyping assay and FCGR3B NA1/2 by the PCR-sequence specific primer (SSP). Allele type, genotype and haplotype of identified polymorphisms were analysed between patients and controls.

Results. Our results revealed that FCGR2A131H/R, FCGR3A176F/V and FCGR3B NA1/2 were not associated with anti-GBM disease. The frequency of the FCGR2B 232T allele (30.2% versus 15.6%, corrected P = 0.00028, 95% CI: 1.42–3.89) and genotypes of I232T (60.4% versus 31.1%, corrected P = 0.0004, 95% CI: 1.78–6.43) was significantly increased in patients compared with controls.

Conclusion. The present study demonstrates the genetic association of polymorphism of FCGR2B (I232T) with susceptibility to anti-GBM disease in Chinese.

Methods. PPi was measured in plasma samples stored from a recent study of vascular calcification in 54 HD patients, 23 peritoneal dialysis (PD) patients and 38 patients with stage 4 chronic kidney disease (CKD). Calcification was quantified in a standardized section of the superficial femoral artery using computed tomography, and PPi was measured by enzyme assay, at both baseline and 1 year.

Results. Baseline plasma PPi was weakly correlated with age and serum phosphate, but not with alkaline phosphatase activity or other biochemical parameters, and did not differ between HD, PD and CKD patients. Both baseline calcification score and change in the calcification score at 1 year decreased with increasing quartiles of plasma PPi. In a multivariate analysis, plasma PPi was independently correlated with baseline calcification (P = 0.039) and the change in calcification (P = 0.029).

Conclusion. Plasma PPi is negatively associated with vascular calcification in end-stage renal disease (ESRD) and CKD but is not affected by dialysis, the mode of dialysis or nutritional or inflammatory status. Although these data are consistent with an inhibitory effect of PPi on vascular calcification, further studies are needed to establish a causal role.

Methods. We evaluated retrospectively the reports of 9,617 renal biopsies, analyzed by the same pathologist, from January 1993 to December 2007.

Results. The 9,617 renal biopsies performed in subjects of all ages in native kidneys. 4,619 were primary glomerulopathies (GN), the most frequent was focal segmental glomerulosclerosis (FSGS, 24.6%), followed by membranous nephropathy (MN, 20.7%), IgA nephropathy (IgAN, 20.1%), minimal change disease (MCD, 15.5%), mesangioproliferative non IgAN (nonIgAN, 5.2%), diffuse proliferative GN (DPGN, 4.7%) and membranoproliferative GN (MPGN, 4.2%). Lupus nephritis was responsible for most cases which etiology was determined, i.e., 950 out of 2,046 cases (45.5%), followed by post infectious GN (18.9%), diabetic nephropathy (8.5%), benign and malignant nephroangiosclerosis (7.3%), haemolytic–uraemic syndrome and thrombotic thrombocytopenic purpura (HUS/TTP), amyloidosis (4.8%) and vasculitis (4.7%). There was a predominance of secondary GN in the North, mostly due to lupus nephritis (LN); FSGS was very common in Northeast (27.7%), Central (26.9%) and Southeast regions (24.1%); IgAN was most frequent in South (22.8%) and MN in North (29.6%); the total prevalence of MPGN was low, and its regional distribution has not changed along the years.

Conclusion. FSGS was the most frequent primary glomerular disease, followed closely by MN and IgAN. The predominance of FSGS is in accordance with recent studies all over the world that revealed its frequency is increasing. Lupus nephritis predominated among secondary GN in most regions, a finding observed in other studies.

Methods. We examined the number of circulating EPCs in 67 continuous ambulatory peritoneal dialysis (CAPD) patients and age- and gender-matched 142 haemodialysis (HD) patients, and 78 subjects without chronic kidney disease. Arterial stiffness was analysed as pulse-wave velocity (PWV) for these patients, and their mutual relationship with circulating EPCs was examined. EPCs were measured as CD34⁺ CD133⁺ CD45^low VEGFR2⁺ cells determined by flow cytometry.

Results. The EPC numbers exhibited a strong correlation (R² = 0.866) with endothelial-colony forming units on culture assay. The levels of EPCs in HD or CAPD subjects were significantly lower than those in control subjects. Among ESRD subjects, the levels of EPC were significantly higher in CAPD subjects than those in HD subjects. In ESRD subjects, PWV levels tended to be associated with EPCs (Rs = –0.131, P = 0.058). However, the significant relationship between dialysis modality and circulating EPCs was independent of the levels of PWV. The association of circulating EPCs with dialysis modality was significant even after adjusting for other potential confounders, including age, gender, blood pressure, history of cardiovascular diseases, presence of diabetes, blood haemoglobin level and treatments with angiotensin-converting enzyme inhibitor/angiotensin II receptor blocker or statin.

Conclusions. CAPD treatment could be a positive regulator of number of circulating EPCs in subjects with ESRD, with the relationship independent of the status of arteriosclerosis.

Methods. Ninety-seven biopsy-proven IgAN patients with moderate histologic lesions, 24-h proteinuria ≥1.0 g and estimated glomerular filtration rate (eGFR) ≥ 50 ml/min/ 1.73 m² were randomly allocated to receive a 6-month course of oral prednisone plus ramipril (combination therapy group) or ramipril alone (monotherapy group) for the total duration of follow-up. The primary outcome was the progression of renal disease defined as the combination of doubling of baseline serum creatinine or end-stage kidney disease (ESKD). The secondary outcomes were the rate of renal function decline defined as the eGFR slope over time, and the reduction of 24-h proteinuria.

Results. After a follow-up of up to 96 months, 13/49 (26.5%) patients in the monotherapy group reached the primary outcome compared with 2/48 (4.2%) in the combination therapy group. The Kaplan–Meier analysis showed a significantly higher probability of not reaching the combined outcome in the combination therapy group than in the monotherapy group (85.2% versus 52.1%; log-rank test P = 0.003). In the multivariate analysis, baseline serum creatinine and 24-h proteinuria were independent predictors of the risk of primary outcome; treatment with prednisone plus ramipril significantly reduced the risk of renal disease progression (hazard ratio 0.13; 95% confidence interval 0.03–0.61; P = 0.01). The mean rate of eGFR decline was higher in the monotherapy group than in the combination therapy group (–6.17 ± 13.3 versus –0.56 ± 7.62 ml/min/ 1.73 m²/year; P = 0.013). Moreover, the combined treatment reduced 24-h proteinuria more than ramipril alone during the first 2 years.

Conclusions. Our results suggest that the combination of corticosteroids and ramipril may provide additional benefits compared with ramipril alone in preventing the progression of renal disease in proteinuric IgAN patients in the long-term follow-up.

Objective. The aim was to assess the long-term efficiency and safety of a monthly oral dose of cholecalciferol (100 000 IU) in vitamin D-deficient haemodialysis (HD) patients.

Methods. HD patients with a serum 25-hydroxyvitamin D (25(OH)D) level <75 nmol/L were enrolled in a 15-month prospective study. The exclusion criteria were as follows: use of any vitamin D derivatives, prescription of cinacalcet and bisphosphonates, uncontrolled hypercalcaemia (>2.55 mmol/L), hyperphosphataemia (>2 mmol/L) and severe secondary hyperparathyroidism (SHPT; serum PTH >600 pg/mL). Biological data were recorded in the following months: M-3, M0, M1, M3, M9 and M15. We aimed to maintain stable levels of the phosphate binder and oral and dialysate calcium during the course of the study.

Results. Of the 250 patients screened, 161 were enrolled, and the results from 107 were recorded at the end of the study. Of these 107 patients, 56% were males, and the average age of the patient group was 66.4 ± 15 years. Diabetics accounted for 36% of the total patients. The dialysis schedule ranged from 3 x 5 to 3 x 8 h, with a mean dialysate calcium concentration of 1.48 ± 0.6 mmol/L. After 15 months, the mean serum 25(OH)D level increased from 32 ± 13 to 105.8 ± 27 nmol/L (P < 0.001) and plateaued after M3. Of the patients, 91% had a level higher than the target level (>75 nmol/L), while none had levels >200 nmol/L. The serum calcitriol (1,25(OH)₂D) level increased from 13.7 ± 14 to 45 ± 13 pmol/L (P < 0.001) and plateaued after M9. The levels of serum PTH (median 295–190 pg/mL, P < 0.001), bone alkaline phosphatase (20.5 ± 9–17.1 ± 7 µg/L, P < 0.05) and β-cross-laps (2.5 ± 1–2.07 ± 0.8 µg/L, P < 0.05) decreased significantly. No significant changes were observed in the values of the following: calcaemia, phosphataemia, blood pressure, serum albumin, haemoglobin and C-reactive protein.

Conclusions. Long-term monthly administration of oral cholecalciferol (100 000 IU) was a safe, effective, inexpensive and simple method for correcting vitamin D deficiency in almost 90% of the HD patients in this study and led to optimal compliance. The most evident consequences were a slight decrease in the levels of PTH and bone markers and an increase in the level of serum 1,25(OH)₂D.

Methods. Thirty-five patients with lupus nephritis and one or more repeat renal biopsies were included. Eighty-four biopsies were blindly reassessed according to the ISN/RPS classification.

Results. Twenty-five patients had one repeat biopsy, 6 patients had two and 4 patients had three repeat biopsies. Forty-nine comparisons between reference and repeat biopsies could be made. In 25 cases (54.3%), there was no shift in ISN/RPS class on repeat biopsies. In 41 instances, paired biopsies showed proliferative lesions both on reference and repeat biopsies, whereas five of six cases with non-proliferative lesions on a reference biopsy switched to proliferative lesions on a repeat biopsy. Clinically significant class switches during lupus nephritis flares were more frequent in patients with non-proliferative lesions in their reference biopsy (P < 0.001).

Conclusion. The results show that patients with proliferative lesions in the original biopsy rarely switch to a pure non-proliferative nephritis during a flare. Therefore, a repeat biopsy during a lupus nephritis flare is frequently not necessary if proliferative lesions were found in the reference biopsy. However, in the case of a non-proliferative lesion in the reference biopsy, class switches are frequently found and repeat biopsies are advisable.

Methods. Renal Association UK Renal Registry data were used to compare the characteristics and survival of patients starting RRT from both groups with those of Caucasians, using incident cases accepted between 1997 and 2006. Survival was analysed by multivariate Cox's proportional hazards regression split by haemodialysis and peritoneal dialysis (PD) due to non-proportionality, and without censoring at transplantation.

Results. A total of 2495 (8.2%) were South Asian and 1218 (4.0%) were Black. They were younger and had more diabetic nephropathy. The age-adjusted prevalence of vascular co-morbidity was higher in South Asians and lower in Blacks; other co-morbidities were generally common in Caucasians. Late referral did not differ. They were less likely to receive a transplant or to start PD. South Asians and Blacks had significantly better survival than Caucasians both from RRT start to Day 90 and after Day 90, and for those on HD or PD at Day 90. Fully adjusted hazard ratios after Day 90 on haemodialysis were 0.70 (0.55–0.89) for South Asians and 0.56 (0.41–0.75) for Blacks.

Conclusion. South Asian and Black minorities have better survival on dialysis. An understanding of the mechanisms may provide general insights for all patients on RRT.

Methods. We prospectively collected data regarding cardiovascular risk factors, clinic and 24-h ambulatory blood pressure monitoring (24-h ABPM) in 98 treated patients with CKD stages 3 and 4.

Results. The mean percentage of systolic blood pressure (SBP) recordings <100 mmHg was 21.2 ± 16.2% and of diastolic blood pressure (DBP) recordings <60 mmHg was 19.8 ± 16.9%. The patients were divided into two groups above and below the median age. The older group had a higher percentage of cardiovascular disease than younger patients (57.1 versus 34.7, P = 0.03) and a lower percentage of primary renal disease (18.4 versus 55.1, P < 0.01). Clinic SBP was higher in the older group (158.4 ± 20.1 versus 147.2 ± 17.8 mmHg, P < 0.01) but 24-h ABPM SBP was not different (117.3 ± 14.7 versus 121.0 ± 12.8 mmHg, P = 0.19). DBP was lower in the older group for both clinic BP (80.3 ± 10.2 versus 85.5 ± 12.3 mmHg, P = 0.03) and 24-h ABPM (69.1 ± 8.2 versus 76.7 ± 8.8 mmHg, P = <0.01). There were a higher percentage of systolic (SBP <100 mmHg) and diastolic (DBP<60 mmHg) hypotensive episodes in the older group (21.3 ± 18.9 versus 13.2 ± 13.6% P = 0.02 and 21.6 ± 17.9 versus 8.1 ± 13.3%, P < 0.01, respectively).

Conclusions. Hypotension was common among treated CKD patients and despite similar clinic SBP, older CKD patients had lower 24-h ABPM DBP and more frequent systolic and diastolic hypotensive episodes. Further research is underway into how this relates to antihypertensive therapy and future outcomes.

Methods. An urban community-based sample of 3714 adults in Shanghai was classified into normal glucose tolerance (NGT), impaired glucose regulation (IGR) and diabetes. The estimated glomerular filtration rate (eGFR) and the urinary albumin-to-creatinine ratio (ACR) were applied to designate renal function and albuminuria, respectively. Binary logistic regression was performed to analyse the contribution of risk factors to CKD. Polynominal regression was used to determine the trends of eGFR with the increment of ACR.

Results. The prevalence of microalbuminuria, macroalbuminuria and CKD in subjects with diabetes was 22.8%, 3.4% and 29.6%, respectively, which was significantly higher than that in non-diabetes subjects. After adjustment for age, the odds ratio of hypertension for albuminuria and renal insufficiency (eGFR <60 mL/min/1.73 m^2, stages 3–5 of CKD) were 1.23 (P = 0.000) and 2.55 (P = 0.000). Diabetes and cardiovascular disease (CVD) both increased the risk for albuminuria significantly, with the odds ratio of 1.22 (P = 0.04) and 1.36 (P = 0.006), respectively. Diabetes and CVD were not independent risk factor for renal insufficiency. Although the worsening trends of eGFR are similar in diabetes and IGR subjects, IGR was not a significant risk factor for albuminuria and renal insufficiency.

Conclusion. Screening for albuminuria and eGFR is highly recommended for older patients with diabetes, hypertension and CVD to prevent end-stage kidney disease.

Methods. Twenty HD patients with PAD were investigated in this study. Clinical effects were evaluated by thermography and angiography. Oxidative stress in serum was evaluated by thiobarbituric acid reactive substances (TBARS) and expression of p22phox mRNA.

Results. Ischaemic symptoms due to PAD were gradually improved in 13 patients (65%) after LDL-A. One session of LDL-A removed ~75% of LDL from serum. Some patients exhibited dramatic improvement of severe symptoms of PAD such as skin ulcers after serial performance of LDL-A. The levels of LDL cholesterol, malondialdehyde-modified LDL, high-sensitivity C-reactive protein, vascular endothelial growth factor, international normalized ratio of pro-thrombin time and bradykinin were decreased after a single session of LDL-A, although there were no additional changes after 10 sessions of LDL-A. The levels of fibrinogen and p22phox mRNA were decreased by a single session of LDL-A, and these decreases continued over the entire period of treatment. TBARS was decreased after a course of LDL-A.

Conclusions. LDL-A improved ischaemic symptoms in HD patients with PAD by reducing ROS production in leucocytes. We conclude that LDL-A is an effective therapy for patients with HD complicated by PAD.

Methods. Patients with class III/IV/V lupus nephritis were included. All patients were on steroids prior to the development of lupus nephritis. Eighteen patients have reached at least 1 year follow-up. These patients received rituximab induction therapy and MMF maintenance therapy. Steroid reduction/withdrawal was guided by clinical response.

Results. Fourteen of 18 (78%) patients achieved complete or partial remission with a sustained response of 12/18 (67%) at 1 year, with 2 patients having a relapse of proteinuria. Four patients did not respond. There was a significant decrease in proteinuria from a mean protein:creatinine ratio (PCR) of 325 mg/mmol at presentation to 132 mg/mmol at 1 year (P = 0.004). Serum albumin significantly increased from a mean of 29 g/L at presentation to 34 g/L at 1 year (P = 0.001). The complication rate was low with no severe infections. Following treatment with rituximab, 6 patients stopped prednisolone, 6 patients reduced their maintenance dose and 6 patients remained on the same dose (maximum 10 mg).

Conclusion. This data demonstrates the efficacy of a rituximab and MMF based regime in the treatment of lupus nephritis, allowing a reduction or total withdrawal of corticosteroids.

Methods. Different methods to detect malnutrition were prospectively investigated for their prognostic impact on mortality and hospitalization of haemodialysis (HD) patients. We compared clinical nutrition scores (body mass index, BMI; subjective global assessment, SGA; malnutrition inflammation score, MIS; and nutritional risk screening, NRS) to lab parameters of protein and lipid metabolism, or bioelectrical impedance analysis (BIA) in 90 HD patients. Over a 3-year follow-up, all-cause mortality and hospitalization were evaluated using a Cox regression model.

Results. The scores SGA, NRS, MIS, serum albumin, prealbumin, transferrin and BIA were predictive of both mortality and hospitalization. Elevated CRP predicted only a significantly higher mortality. After adjustment for age, gender, dialysis vintage and diabetes status, the best prognostic parameters for mortality were the clinical nutrition scores, MIS-Index ≥ 10 [HR 6.25 (2.82–13.87), P < 0.001], NRS [HR 4.24 (1.92–9.38), P < 0.001] and SGA B/C [HR 2.70 (1.14–6.41), P < 0.05].

Conclusions. In HD patients, serum markers of protein metabolism and BIA can be used for evaluation of the nutritional status. However, with regard to mortality and hospitalization risk, the individual clinical nutrition scores are superior compared to lab markers and BIA. To confirm malnutrition, we propose using clinical nutrition score generally or at least in the case of two malnutrition-positive parameters (lab, BIA, BMI).

Methods. CXCL13 was measured in sera obtained from 91 patients with SLE and 40 healthy controls by ELISA methodology. Disease activity was calculated according to the SLE Disease Activity Index (SLEDAI).

Results. Median (IQR) serum CXCL13 concentrations were increasingly higher across the following groups: healthy controls [31.6 (26.8–41.3) pg/ml], SLE patients with inactive disease (SLEDAI <6) [68.2 (27.8–133.0) pg/ml, P = 0.0006 versus controls] and active disease [196.0 (75.9–416.8) pg/ml, P = 0.0001 versus controls] (inactive versus active P < 0.0001). Concentrations of circulating CXCL13 correlated with SLEDAI (r = 0.56, P < 0.0001) and double-stranded DNA titres (r = 0.36, P < 0.0005). Moreover, median CXCL13 concentrations were higher in patients with renal involvement [175.5 (105.3–422.6) pg/ml] compared to those without renal involvement [82.1 (42.9–219.8) pg/ml].

Conclusions. Our data indicate that increased level of CXCL13 is a feature of SLE that correlates with disease activity. Furthermore, CXCL13 might be a readily available surrogate marker to monitor the extent of aberrant B-cell (dys-)function.

Patients and methods. Eighteen patients with body mass index (BMI) >50 kg/m² who underwent a variant of biliopancreatic diversion with Roux-en-Y reconstruction (BPD-RYGBP) and consented to undergo a renal biopsy during the surgical procedure were included in the study. The estimation of early histological changes was performed on light (n = 18) and electron microscopy (n = 13).

Results. The mean glomerular cross-sectional area was 30 943 ± 10 984 µm² that is higher than that observed in non-obese individuals. In 21% of the examined glomeruli, the glomerular planar surface area (GPSA) was >40 000 µm². Thickening of the glomerular basement membrane (GBM) and scattered paramesangial deposits were identified in 9 of 13 patients (70%) whose renal tissue was examined by electron microscopy. A reduction in the slit pore frequency was observed in obese patients due to extensive foot process effacement. Significant positive correlations between mean GPSA and body weight (r = 0.462, P = 0.05), and between GBM thickness and HbA1c, serum total cholesterol and triglyceride levels (r = 0.60, P = 0.05; r = 0.789, P = 0.004; r = 0.70, P = 0.016, respectively), were observed.

Conclusions. Glomerulomegaly as well as histological lesions resembling those of early diabetic nephropathy are observed in kidney biopsies of patients with morbid obesity even before the appearance of microalbuminuria. The potential regression of these changes after weight loss needs to be clarified.

Methods. MEDLINE (1950–May 2009), EMBASE (1980–May 2009) CENTRAL (up to May 2009) and bibliographies of retrieved articles were searched for relevant RCTs. Analysis was by a random effects model and results expressed as rate ratio, relative risk (RR) and weighted mean difference (WMD) with 95% confidence intervals (CI).

Results. A total of 29 trials with 2886 patients and 3005 catheters were included. Antimicrobial catheter locks (AMLs) significantly reduced the rates of CRBs (rate ratio, 0.33, 95% CI 0.24–0.45) and exit-site infections (ESIs) (rate ratio 0.67, 95% CI 0.47–0.96). Exit-site antimicrobial application also significantly reduced the rates of CRBs (rate ratio 0.21, 95% CI 0.12–0.36) and ESIs (rate ratio 0.22, 95% CI 0.10–0.47). Antimicrobial coating of HD catheters and the use of peri-operative antimicrobials did not result in significant reduction in rates of CRBs and ESIs.

Conclusion. The use of AMLs and exit-site antimicrobials are useful measures in the reduction of CRIs, whereas antimicrobial impregnated catheters and peri-operative systemic antimicrobial administration have not been found to be beneficial. Further head-to-head trials of various AMLs and exit-site antimicrobials are needed to know about their comparative clinical efficacy.

Methods. This is an open randomized clinical trial. Hypertensive patients on haemodialysis were randomized to have the antihypertensive therapy adjusted based on predialysis BP measurements or HBPM. Before and after 6 months of follow-up, patients were submitted to ambulatory blood pressure monitoring (ABPM) for 24 h, HBPM during 1 week and echocardiogram.

Results. A total of 34 and 31 patients completed the study in the HBPM and predialysis BP groups, respectively. At the end of study, the systolic (SBP) and diastolic (DBP) blood pressure during the interdialytic period measured by ABPM were significantly lower in the HBPM group in relation to the predialysis BP group (mean 24-h BP: 135 ± 12 mmHg/76 ± 7 mmHg versus 147 ± 15 mmHg/79 ± 8 mmHg; P < 0.05). In the HBPM analysis, the HBPM group showed a significant reduction only in SBP compared to the predialysis BP group (weekly mean: 144 ± 21 mmHg versus 154 ± 22 mmHg; P < 0.05). There were no differences between the HBPM and predialysis BP groups in relation to the left ventricular mass index at the end of the study (108 ± 35 g/m² versus 110 ± 33 g/m²; P > 0.05).

Conclusions. Decision making based on HBPM among haemodialysis patients has led to a better BP control during the interdialytic period in comparison with predialysis BP measurements. HBPM may be a useful adjuvant instrument for blood pressure control among haemodialysis patients.

Methods. A total of 210 cases of adult primary FSGS diagnosed during 4 years (May 2002 to June 2006) were categorized into the variants and their presentation and morphological details were compared. Renal biopsies were studied by light microscopy, immunofluorescence/immunohistochemistry and electron microscopy.

Results. In the present study, the frequency of various morphological variants was collapsing 2%, tip 13.5%, cellular variant 8%, perihilar 4% and FSGS-NOS 72.5%. The variants had a significant difference in the duration of onset of illness at the time of biopsy. The cellular variants were biopsied the earliest (4.38 ± 5.57 months) followed by collapsing (10.75 ± 16.88 months) and perihilar variant at a later stages (65.33 ± 99.30 months). The difference in the degree of proteinuria was statistically significant (P = 0.017) amongst various variants, being highest in collapsing variant (6.17 ± 4.67 g/day) and lowest in perihilar variant (1.94 ± 0.94 g/day).

Conclusion. The present study highlights that there is difference in the prevalence and some of the clinical parameters at the time of presentation in Indian patients. There was lower prevalence of perihilar variant and a higher prevalence of tip and cellular variants taken together when compared with the western literature, and this was similar to observations of another Asian cohort (China). Collapsing variant was infrequent when compared to the west.

Methods. We performed a 4-year prospective follow-up study in 231 chronic PD patients from a single regional dialysis centre in Hong Kong. Valvular calcification was detected using echocardiography, and fasting venous blood was collected to measure a panel of inflammation markers. The patients were stratified into five groups on the basis of 0, 1, 2, 3 and all 4 inflammation and calcification risk markers, namely high C-reactive protein (CRP) (CRP in upper tertile), high interleukin-6 (IL-6) (IL-6 in upper tertile), low fetuin-A (fetuin-A in lower tertile) and valvular calcification. Study outcomes included all-cause and cardiovascular mortality and fatal or non-fatal cardiovascular events (CVEs).

Results. The patients with 4, 3, 2 and 1 markers had an adjusted hazard ratio (HR) of 5.17 (95% CI, 1.81–14.77, P = 0.002), 3.38 (95% CI, 1.50–7.60; P = 0.003), 2.17 (95% CI, 0.98–4.77; P = 0.056) and 2.42 (95% CI, 1.18–4.96; P = 0.016), respectively, for mortality at 4 years than those with 0 risk marker. The adjusted HRs for fatal or non-fatal CVEs were 4.33 (95% CI, 1.70–11.03; P = 0.002), 1.60 (95% CI, 0.73–3.52; P = 0.24), 1.92 (95% CI, 0.95–3.90; P = 0.07) and 1.33 (95% CI, 0.67–2.62; P = 0.42), respectively, for patients with 4, 3, 2 and 1 markers than those with 0 risk markers.

Conclusions. A composite of inflammation and calcification markers provides long-term prognostication and identifies the sickest PD patients with the worst clinical outcomes. Since these parameters can all be obtained quite readily, our data support the adoption of a multiinflammation and calcification risk marker approach for mortality and cardiovascular risk stratification in PD patients.

Methods. A population-based study linking all women attending the Second Health Study in Nord-Trøndelag, Norway (1995–97) and subsequent pregnancies registered in the Medical Birth Registry. Multivariable random-effect logistic regression analysis was used to explore the association between renal function and study outcome.

Results. The mean eGFR among 3405 women was 107.6 ± 19.4 ml/min/1.73 m² at baseline; 18.8% and 0.1% had eGFR of 60–89 and <60, respectively. Over the next 11 years, they gave birth to 5655 singletons of whom 885 (17.7%) were complicated with preeclampsia, small for gestational age (SGA) or preterm birth. Women with eGFR 60–89 were not at increased risk for this combined outcome compared to women with eGFR ≥90, although women with eGFR 60–74 tended to have an increased risk. Neither was reduced kidney function a risk factor among women with microalbuminuria, but those with an eGFR of 60–89 plus hypertension had a significantly increased risk: odds ratios for preeclampsia, SGA or preterm birth were 2.58 (95% CI 1.40–4.75, P < 0.001) and 10.09 (95% CI 2.38–42.87, P < 0.001) in hypertensive women with eGFR 75–89 and 60–74, respectively. Relative excess risk due to interaction between reduced kidney function and hypertension was 2.23 (95% CI 1.35–3.10, P < 0.001). Women with a reduced kidney function were not at increased risk for other pregnancy complications like caesarean section, maternal bleeding, dystocia, pre-labour rupture of membranes, Apgar score ≤7, stillbirth or congenital malformations.

Conclusions. Women with eGFR 60–89 ml/min/1.73 m² were not at increased risk for preeclampsia, SGA or preterm birth unless they were also hypertensive.

Methods. We investigated the frequency, predictors, treatment and clinical outcomes of Corynebacterium peritonitis in all Australian adult patients involving 66 centres who were receiving PD between 1 October 2003 and 31 December 2006.

Results. Eighty-two episodes of Corynebacterium peritonitis (2.3% of all peritonitis episodes) occurred in 65 (1.4%) PD patients. Ten (15%) patients experienced more than one episode of Corynebacterium peritonitis and additional organisms were isolated in 12 (15%) episodes of Corynebacterium peritonitis. The incidence of Corynebacterium peritonitis was significantly and independently predicted only by BMI: RR 2.72 (95% CI 1.38–5.36) for the highest tertile BMI compared with the lowest tertile. The overall cure rate with antibiotics alone was 67%, which was similar to that of peritonitis due to other organisms. Vancomycin was the most common antimicrobial agent administered in the initial empiric and subsequent antibiotic regimens, although outcomes were similar regardless of antimicrobial schedule. Corynebacterium peritonitis not infrequently resulted in relapse (18%), repeat peritonitis (15%), hospitalization (70%), catheter removal (21%), permanent haemodialysis transfer (15%) and death (2%). The individuals who had their catheters removed more than 1 week after the onset of Corynebacterium peritonitis had a significantly higher risk of permanent haemodialysis transfer than those who had their catheters removed within 1 week (90% versus 43%, P < 0.05).

Conclusions. Corynebacterium is an uncommon but significant cause of PD-associated peritonitis. Complete cure with antibiotics alone is possible in the majority of patients, and rates of adverse outcomes are comparable to those seen with peritonitis due to other organisms. Use of vancomycin rather than cephazolin as empiric therapy does not impact outcomes, and a 2-week course of antibiotic therapy appears sufficient. If catheter removal is required, outcomes are improved by removing the catheter within 1 week of peritonitis onset.

Methods. We explored the cross-sectional association between duration of PMH use and albuminuria in 2445 post-menopausal, non-diabetic women from the Nurses’ Health Study. Women were categorized as hormone non-users, past users or current users grouped by 3-year intervals of duration of use, from ≤3 years to >15 years. The outcome was the top decile of urine albumin/creatinine ratio (ACR). Multivariate logistic regression was used to assess the association between duration of PMH use and risk of being in the top decile.

Results. The mean age was 66.8 years, and 57% were currently using PMH. The median ACR was 2.9 mg/g, and the 90th percentile was 9.2 mg/g. Compared with women with no history of PMH use, the odds ratio for being in the top ACR decile was lower for women with use of >6–9 years, >9–12 years, >12–15 years and >15 years, but there was no dose–response. The overall odds ratio was 0.55 (95% CI: 0.39–0.77) among women with >6 years of current PMH use compared with non-users. Current hormone use of shorter duration and past hormone use were not associated with albumin excretion.

Conclusions. Current PMH use of >6 years is associated with a lower urinary ACR in non-diabetic women.

Methods. Over a period of 7 years, 74 consecutive patients underwent angiography of an immature fistula that showed either stenosis or an insufficient enlargement of the radial artery that was treated by percutaneous dilation. Success, complications and secondary interventions were recorded according to consensus definitions. Patency following angioplasty was estimated with the Kaplan–Meier technique.

Results. The mean patient age was 70 years, 44% were women, 69% had diabetes, 23% were smokers, 76% had hypertension, 64% had coronary disease and 46% had peripheral artery occlusive disease. Concomitant venous stenosis was diagnosed in 53% of patients. Arterial stenosis was >5 cm long in 53 cases. Technical success was achieved in 73/74 cases following angioplasty. All but two fistulas were then successfully used for dialysis. Dilation-induced rupture occurred in 13 cases (17%) but required only two stent placements. Five cases (7%) of hand ischaemia within 1 month of dilation were treated successfully by ligation of the distal artery. Primary patency rates at 12 and 24 months were significantly better for pure arterial lesions, with 65% and 61% compared to 42% and 35% in cases of concomitant venous stenosis (P < 0.04). The secondary patency rates were 96% and 94% at 1 and 2 years, respectively.

Conclusion. Dilation of the radial artery yields higher patency rates than for veins. Surgeons might therefore be less demanding about the initial quality of the radial artery prior to creation of radial-cephalic fistulas.

Methods. The Polymorphism REsearch to DIstinguish genetic factors Contributing To progression of IgAN (PREDICT-IgAN) was a multicentre retrospective observational study to investigate associations between progression of IgAN (a 50% increase of serum creatinine level and slope of eGFR) and a hundred atherosclerotic disease-related gene polymorphisms, mainly single nucleotide polymorphisms (SNPs) in 320 IgAN patients who had more than a normal range of urinary protein (≥0.25 g/day) at diagnosis.

Results. During 8.3 ± 4.2 years of a follow-up period, 83 patients (25.9%) developed progression. In log-rank tests, glycoprotein Ia GPIa C807T and G873A and intercellular adhesion molecule-1 ICAM-1 A1548G (K469E) were found to be significantly associated with progression even after adjustment for multiple comparisons by the method of Bonferroni (adjusted P = 0.0174, 0.0176 and 0.0430, respectively). In a multivariate Cox proportional-hazards model, GPIa 807TT (873CC) [versus 807TT, adjusted hazard ratio 2.05 (95% confidence interval 1.13–3.71)] and ICAM-1 1548GG [versus 1548AA, 2.55 (1.40–4.65)] were identified as independent genetic predictors of progression, along with conventional clinical prognostic factors such as eGFR, urinary protein and use of antihypertensives at diagnosis.

Conclusions. PREDICT-IgAN distinguished GPIa C807T/ G873A and ICAM-1 A1548G from multiple athero- sclerotic disease-related gene polymorphisms by their predictive indicator for progression of IgAN.