Progressive renal fibrosis resulting from proliferation of interstitial fibroblasts is a hallmark of chronic kidney failure, whatever the origin. The intermediate/small-conductance Ca²⁺-activated K⁺ channel (K_Ca3.1) promotes mitogenesis in several cell types by altering the membrane potential, thus enabling extracellular Ca²⁺ entry. Grgic et al. evaluated the role of K_Ca3.1 in renal fibroblast proliferation, testing whether deficiency or pharmacological blockade of K_Ca3.1 suppressed development of renal fibrosis. Mitogens stimulated K_Ca3.1 in murine renal fibroblasts via a MEK-dependent mechanism, while selective blockade of K_Ca3.1 inhibited fibroblast proliferation by promoting G0/G1 arrest. In a classical model of renal fibrosis, mouse unilateral ureteral obstruction (UUO), robust up-regulation of K_Ca3.1 was detectable in affected kidneys. K_Ca3.1 KO mice showed reduced expression of fibrotic marker expression, less chronic tubulointerstitial damage, collagen deposition and -smooth muscle+ cells after UUO, with better preservation of functional renal parenchyma. The selective K_Ca3.1 blocker TRAM-34 similarly attenuated progression of UUO-induced renal fibrosis in wild-type mice and rats. Thus, Grgic et al. believe that K_Ca3.1 is involved in renal fibroblast proliferation and fibrogenesis, suggesting that K_Ca3.1 may serve as a therapeutic target for the prevention of fibrotic kidney disease.

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. 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. 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. 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. 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. 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. 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. 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. 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.

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. 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. 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. 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 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. 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. 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. 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. 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. 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. 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. 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.

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. 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. 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. 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. 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. 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. 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. 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.

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. 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. 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. 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. 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.

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.

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. 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. 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.

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. 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.

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.