Skip Navigation


NDT Advance Access originally published online on April 27, 2006
Nephrology Dialysis Transplantation 2006 21(9):2615-2620; doi:10.1093/ndt/gfl211
This Article
Right arrow Abstract Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow All Versions of this Article:
21/9/2615    most recent
gfl211v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (6)
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Schwarz, C.
Right arrow Articles by Haas, M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Schwarz, C.
Right arrow Articles by Haas, M.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© The Author [2006]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Original Articles: Dialysis and Transplantation

Complete renal tubular acidosis late after kidney transplantation

Christoph Schwarz1, Thomas Benesch2, Katharina Kodras1, Rainer Oberbauer1 and Martin Haas1

1 Department of Internal Medicine III, Division of Nephrology and Dialysis and 2 Department of Medical Statistics, University Hospital Vienna, Austria

Correspondence and offprint requests to: Martin Haas, MD, Department of Internal Medicine III, Division of Nephrology, University Hospital Vienna, Währinger Gürtel 18–20, 1090 Vienna, Austria. Email: martin.haas{at}meduniwien.ac.at



   Abstract
Top
 Abstract
Introduction
 Subjects and methods
 Results
 Discussion
 References
 
Background. Neither the prevalence nor the associated risk factors of late post-transplant renal tubular acidosis (RTA) are known.

Methods. We conducted a cross-sectional study with 576 patients for more than 12 months after kidney transplantation, and a glomerular filtration rate (GFR) >40 ml/min. RTA was diagnosed by measurement of the urine anionic gap, urine pH and plasma potassium during acidosis, and fractional bicarbonate excretion after bicarbonate loading. Uni- and multi-variable analysis were used to isolate factors associated with post-transplant RTA, and with the different RTA subtypes.

Results. All patients (n = 76) had distal post-transplant RTA. A significant association with the presence of RTA was found for the intake of tacrolimus or renin–angiotensin–aldosterone blockers, the Parathyroid hormone level and the GFR. Type Ia (classic, distal), type Ib (hyperkalaemic, voltage-dependent), rate-limited and type IV RTA were present in 37, 14, 21 and 28% of the patients. Acute transplant rejection was the only significant different parameter between the RTA subtypes and more often present in patients with type Ia or Ib RTA.

Conclusions. We conclude that a significant fraction of stable long-term renal transplant recipients with adequate graft function develop post-transplant RTA, with a preponderance for type Ia and type IV, and absence of type II. In addition, acute transplant rejection seems to have an influence on the subtype of RTA present post-transplantation.

Keywords: acute rejection; renal tubular acidosis; transplantation



   Introduction
Top
 Abstract
 Introduction
Subjects and methods
 Results
 Discussion
 References
 
The first description of a patient with post-transplant renal tubular acidosis (RTA) was published by Massry et al. [1], almost three decades ago. Several smaller case series have been published since then [2–11], but only one study investigated the course of post-transplant RTA in a larger population [8]. Thus, the incidence and cause of post-transplant RTA is mainly unknown.

Transplantation-associated RTA can be roughly classified according to the time point of its appearance. During the early course post-transplantation, type II (proximal) RTA seems to prevail. This form of RTA is characterized by bicarbonate wasting due to the toxic effects of calcineurin inhibitors or persisting hyperparathyroidism [12,13]. During the first 6 months post-transplantation, however, as the tubular damage and hyperparathyroidism resolves, RTA improves and might completely mend [5–8]. In contrast, distal or type I RTA (dRTA), which is characterized by the inability to excrete hydrogen ions, either persists or occurs as a de novo disease late after the transplantation [8]. Distal RTA has been suspected to be associated with interstitial damage caused by chronic transplant rejection or long-term intake of calcineurin inhibitors [14]. Three major forms have been described in transplant recipients, the classic type Ia, the hyperkalaemic type Ib (voltage-dependent) and a mixed form with additional bicarbonate wasting (type III). Type IV RTA is mainly caused by drugs suppressing the renin–angiotensin–aldosterone system (RAAS), and thus, although occurring after transplantation, not directly associated with graft dysfunction.

Despite the knowledge about the different forms of post-transplant RTA, a description of their prevalence, the prevalence of the different subtypes and of the associated factors is still lacking. It is furthermore unclear whether transplant-associated RTA resembles hereditary RTA. This cross-sectional study was performed to investigate the prevalence and subtypes of acid–base disorders in stable renal allograft recipients.



   Subjects and methods
Top
 Abstract
 Introduction
 Subjects and methods
Results
 Discussion
 References
 
All transplant recipients treated at the out-patient clinic of the Department of Nephrology, University Hospital Vienna, with a glomerular filtration rate (GFR) >40 ml/min, measured with the abbreviated modification of diet in renal diseases (MDRD) formula [GFR (ml/min/1.73 m2) = 186 x (serum creatinine) (–1.154) x (age) (–0.203) x (0.742, if female) x (1.212, if African-American)], and a transplant duration greater than one year (n = 589) were asked to participate in this study. Exclusion criteria were an acute graft rejection or dysfunction <6 months prior to the study entry, chronic or acute diarrhoea, urinary diversion (i.e. transabdominal diversion of the urine through a segment of the intestine), neoplasm of any kind, severe liver disease and acute urinary tract infection. Five patients refused to give informed consent, another five had received a urinary diversion prior to the transplantation and three patients had chronic diarrhoea, thus a total of 576 patients were included. The study was approved by the local institutional review board (IRB) and all patients gave their informed consent.

The patients were screened for RTA by two independent determinations of pH, bicarbonate and electrolytes (potassium, sodium, calcium, chloride and phosphate) in the venous blood after discontinuation of bicarbonate and furosemide therapy. In 15 patients, venous and arterial blood gas analysis were compared in order to exclude an influence of decreased systemic or muscle blood flow. Urine electrolytes were measured in a sample from a 24 h-urine collection, and urine pH in fresh urine specimens sampled in vacuum tubes immediately after blood collection. The measurements were done after collection with the ABL 700 blood gas analyser (Radiometer, Copenhagen, DK). Electrolytes were measured by the standard laboratory means. Before a second control, all acidotic patients received an oral bicarbonate load of 5–10 g in the prior evening and 2 h before analysis. If blood bicarbonate was <22 mmol/l, the test was repeated with a higher bicarbonate dose.

For the diagnosis of the RTA subtypes the serum-potassium concentration and the following markers were calculated at the same day as bicarbonate measurement (Table 1; modified from [14]):

  1. The plasma anionic gap (PAG) = Na+ – Formula – Cl– (normal: 8–16 mmol/l). A normal PAG in combination with a decreased serum pH (<7.35) and decreased bicarbonate concentration was considered as metabolic acidosis.
  2. In order to estimate ammonium excretion, the urine anionic gap (UAG) was calculated from a 24 h urine specimen as UAG = (Na+ + K+) – Cl–, after exclusion of exsiccosis (i.e. a urinary sodium <25 mmol/l), diarrhoea and ketoacidosis. Classic (Ia) and hyperkalaemic (Ib)-dRTA have a positive UAG and a urine pH >5.5, and differ only by the serum-potassium concentration. The rate-limited RTA is characterized by impaired ammonium secretion but the ability to acidify the urine. It differs from type Ia by the urine pH (which is below 5.5) and from Ib additionally by a normal serum-potassium concentration [14].
  3. For the diagnosis of proximal (type II) RTA, the fractional excretion of bicarbonate was calculated as FeHCO3 = (UHCO3 x PCr/PHO3 x UCr) x 100 during acidosis and after bicarbonate loading. UHCO3 and UCr stand for urine bicarbonate and urine creatinine, and PHCO3 and PCr for plasma bicarbonate and plasma creatinine concentration. In addition, the total reabsorption of phosphate (TRP) was calculated as: TRP = [1 – (UPh x SCr)/(SPh x UCr)] x 100, where UPh is urine-phosphate concentration and SPh serum-phosphate concentration, and the fractional excretion of potassium (FeK) with the same equation as the FeHCO3.


View this table:
[in this window]
[in a new window]

  		Table 1. Diagnosis of renal tubular acidosis

 
Parameters that might influence the development of post-transplant RTA were obtained from all patients. These were: age, sex, MDRD-GFR, drug intake [ciclosporine A, tacrolimus, rapamycin, mycophenolate mofetil, azathioprine, prednisolone, furosemide, thiazides and blockers of the RAAS (RAAB)], number of transplantations, previous rejections, diabetes, donor status (deceased or living) and intact parathyroid hormone (iPTH) level. These factors were compared between patients with and without RTA, and between the RTA subtypes.

Statistical analysis
The results are given as mean ± SD. We performed a univariable analysis with the unpaired t-test for continuous data, and the chi-square test or Fisher's exact test for categorical data, between patients with and without RTA. Thereafter, a multivariable logistic regression was performed with those variables, which, according to the univariable analysis, most likely would have an influence on the development of RTA. For the analysis between the RTA types, a univariable analysis of variance for continuous data and a chi-square test for categorical variables were used. A subsequent multivariable analysis was performed with a multinomial regression.

A multivariable general logistic regression analysis was used to evaluate which factors are predictive for the four different RTA types compared with no RTA. The co-variables were selected on the basis of clinical experience (ciclosporine A, tacrolimus, furosemide, thiazides, RAABs, PTH level, acute rejection and transplant age). We applied a two-sided significance level of <0.05.



   Results
Top
 Abstract
 Introduction
 Subjects and methods
 Results
Discussion
 References
 
RTA was diagnosed in 76 out of 576 patients (13%), and was treated with sodium bicarbonate in all [mean (SD) dose: 2.4 ± 1.2 g/day]. The correlations (R2) between arterial and venous pH, Formula, and base excess (BE) in 15 randomly selected patients were 0.93, 0.94 and 0.95. Only pO2 differed significantly between arterial and venous samples, but none of the other blood gas values.

In the univariable analysis, patients with RTA were younger, had shorter transplant duration, a lower MDRD-GFR, a higher PTH level, a higher number of previous transplantations, more often tacrolimus as an immunosuppressant, and more often RAAB blockers (Table 2). In the subsequent multivariable logistic regression analysis, a significant difference was found for iPTH level, MDRD-GFR, and tacrolimus or RAAB intake (Table 2). The odds ratios (OR) and 95% confidence intervals (CI) were: MDRD-GFR 1.02 (1.005–1.040), for PTH 0.996 (0.993–1.0), for RAAB 2.1 (1.21–3.66) and for tacrolimus 1.98 (1.11–3.52).


View this table:
[in this window]
[in a new window]

  		Table 2. Differences between transplant recipients with and without RTA

 
RTA developed in 32 of 76 patients immediately after transplantation and in 44 of 76 during the later post-transplant course. Of the latter, 22 (49%) had had an acute transplant rejection prior to the development of RTA.

None of the patients had proximal RTA (type II). This was evidenced by the positive UAG in all groups and the low fractional excretion of bicarbonate (Table 3). The main types were the classic type Ia (37%) and type IV RTA (28%). These were followed by the rate-limited distal RTA (21%) and the hyperkalaemic type Ib RTA (14%). As expected, patients with type Ia and Ib RTA were unable to acidify the urine (UpH >5.5), with additional hyperkalaemia in type Ib patients. Those with the rate-limited distal RTA and type IV RTA were able to acidify the urine to a pH <5.5, and differed only by serum-potassium values (Table 3). Despite the elevated potassium levels in type Ib and type IV RTA, the fractional excretion of potassium (FeK) was within the normal range in all groups, and thus inadequately low in patients with high potassium RTA. The impaired potassium excretion in the hyperkalaemic patients was confirmed by the measurement of the transtubular potassium gradient in 18 of 32 patients, which was decreased (<8) in all. A 24 h urinary excretion of calcium, which is usually increased in native kidney dRTA, was clearly below normal in all the four groups. TRP, a measure for tubular phosphate handling, was also reduced in all types of RTA.


View this table:
[in this window]
[in a new window]

  		Table 3. Parameters of metabolic acidosis and electrolytes in the RTA subtypes (mean ± SD)

 
The number of acute rejections was significantly higher in classic type Ia and hyperkalaemic type Ib RTA than in the rate-limited or type IV RTA (Table 4). This difference was the only significant discriminating factor in the univariable analysis between the four groups, which was performed with the same parameters as previously described. A multivariable stepwise-logistic regression analysis with transplant age, PTH level, the intake of RAAB and previous acute rejections confirmed the effect of acute rejections as the only discriminating factor (Table 4).


View this table:
[in this window]
[in a new window]

  		Table 4. Differences between RTA subtypes

 
Only RAAB, PTH, acute rejection and transplant age could significantly predict a subtype of dRTA compared with no RTA. Type IV dRTA was predicted by RAAB intake [OR (95%CI): 7.9(1.79–35); P < 0.01), type Ia dRTA by the PTH level [1.007(1.001–1.013) for each ng/ml increase of PTH; P < 0.05] and the acute rejection [2.72 (1.57–4.72); P < 0.001], and the rate-limited dRTA by transplant age [0.86 (0.74–0.99) for each year; P < 0.05].



   Discussion
Top
 Abstract
 Introduction
 Subjects and methods
 Results
 Discussion
References
 
Our results show that almost 13% of all long-term kidney transplant recipients with a functioning graft have distal RTA. Furthermore, that proximal RTA, which has been described to occur shortly after kidney transplantation [1,2,5–8], resolves subsequently. This finding is in accordance with the report of Wilson and Siddiqui [8], which until now was the only investigation on late post-transplant RTA. The study, however, differs substantially from ours. Tubular bicarbonate handling, which is necessary for the differentiation between proximal and distal RTA, was only measured in two patients, and the different dRTA subgroups were not described. In addition, neither RTA as a group nor the subgroups were correlated to possible pathognomonic factors.

Since graft function deteriorated more rapidly in affected patients, the authors suggested that chronic rejection might influence post-transplant dRTA. Interestingly, we too found a significantly worse graft function, despite shorter graft duration, in patients with dRTA, this however could not have been the cause of RTA, since all patients had a GFR >40 ml/min, which precludes acidosis of chronic renal failure [15], nevertheless other causes influencing glomerular and tubular function must have been more present in patients with RTA. The most likely are nephrotoxic immunosuppressives like tacrolimus or (sub)clinical rejection. The latter is supported by the finding, that the majority of the patients with metabolic acidosis presented with classic dRTA (type Ia). This type is characterized by a defect of the H+-ATPase [15–17] which, among others, can also be caused by auto-antibodies [18–20]. Similar antibodies could be present after kidney transplantation, which is supported by the finding that significantly more patients with a defect of H+-ATPase (Ia or Ib dRTA) had acute rejection than patients with rate-limited or type IV RTA. Immunohistochemical staining of the H+-ATPase has actually been performed in kidney transplant recipients with acute rejection, but revealed no specific loss [10]. The study, however, is hampered by several factors. The number of patients was low, the majority had a serum-creatinine >2 mg/dl and almost no patient had a low urine pCO2, a characteristic feature of impaired H+ secretion. Thus, a direct effect of acute graft rejection on the H+-ATPase could nevertheless be possible and should be further investigated.

For the diagnosis of dRTA measurement of the urine–blood, pCO2 has also been suggested [21], which, however, is hampered by the variability of bicarbonate in the urine, and thus rejected by others [16]. Measurement of pCO2 might be particularly unspecific in kidney transplant recipients, since most grafts have a tubular concentration defect. Thus, in our opinion determination of the UAG and urine pH, which both have a high sensitivity [16], is sufficient for the diagnosis of the subtype of post-transplant dRTA.

A special form of dRTA with a normal potassium level is the rate-limited dRTA. In contrast to the classical dRTA, the urine pH can be lowered below 5.5 during acidosis, or after an acid load, and shows a normal response to phosphate infusion [22]. The subsequent evolution of the rate-limited dRTA is currently unknown. It might be an early form of the classical type 1 RTA, or improve, as reported in the study of Wilson and Siddiqui [8]. The latter, however, is closely correlated to the improvement of kidney function after transplantation, which is unlikely in our patients. Late post-transplant rate-limited dRTA might, therefore, rather result from chronic interstitial changes due to transplant failure. Continuous follow-ups will hopefully reveal the further course.

The significant association of higher parathyroid hormone levels with dRTA can be interpreted as either a consequence or a cause of metabolic acidosis. Hyperparathyroidism in secondary native kidney RTA has an influence on both proximal as well as distal RTA [14,17]. The cause for the latter is the associated hypercalciuria which influences the H+-gradient across the distal tubule which impairs hydrogen excretion. Our study patients, however, had a decreased 24 h calcium excretion, which contradicts the assumption of an association between dRTA and hyperparathyroidism. This unusual finding might be explained by post-transplant PTH resistance of the bone [23], but not the graft, which has been taken from a normal environment. Due to the different responses to PTH, calcium mobilization from bone will be reduced and tubular calcium reabsorption is enhanced resulting in hypocalciuria despite hyperparathyroidism. Synthesis of 1,25(OH2) vitamin D3 [24], on the other hand, is reduced by acidosis, which in turn increases PTH synthesis. In addition, calcium sensing of parathyroid cells is decreased by acidosis, which also stimulates PTH secretion [25]. Considering these effects it therefore, seems to be more likely that acidosis contributes to hyperparathyroidism than the contrary. This in turn shows the importance of effective treatment of metabolic acidosis. Besides hyperparathyroidism, acidosis has a broad range of different adverse effects [26]. In particular, protein degradation and bone disease can lead to long-term complications.

Interestingly, the lack of association occurs with cyclosporine but not tacrolimus, which also has been described in a smaller study by Heering et al. [11]. Ciclosporine causes incomplete dRTA in animals [27] as well as in humans [28,29], which, since we only investigated the complete RTA, might have been the reason for missing a correlation. The influence of ciclosporine on incomplete dRTA can be explained by a study of Watanabe et al. [30]. In this, the acidosis-induced transformation of the tubular ß-intercalated cells, which secrete bicarbonate, into {alpha}-intercalated cells, which secrete hydrogen, is described to be inhibited by cyclosporine but not tacrolimus. Inhibition of the cell transformation prevents an increased hydrogen secretion after an acid load. Since the number of ß-intercalated cells remains unchanged, bicarbonate excretion will continue with the same rate, which results in the classical dRTA (high urinary pH during metabolic acidosis). Tacrolimus did not influence cell transformation and must therefore, regarding the significant influence found in our study, exert a different and more pronounced effect on tubular function.

In summary, we were able to demonstrate a significant prevalence of distal renal tubular acidosis in long-term kidney transplant recipients with adequate graft function. Furthermore, the tacrolimus therapy has a more pronounced effect on the development of dRTA than cyclosporine, and the treatment with a RAAB is responsible for dRTA in approximately 25% of the patients. Finally, since acute rejection seems to play a major role for the type of dRTA, it might be possible that a direct immunological action, for example by specific antibodies, influences the secretory capacity of the intercalated cells.

Conflict of interest statement. None declared.



   References
Top
 Abstract
 Introduction
 Subjects and methods
 Results
 Discussion
 References
 

  1. Massry SG, Preuss HG, Maher JF, Schreiner GE. Renal tubular acidosis after cadaver kidney homotransplantation. Am J Med 1967; 42: 284–292[CrossRef][ISI][Medline]
  2. Gyory AZ, Stewart JH, George CR, Tiller DJ, Edwards KD. Renal tubular acidosis, acidosis due to hyperkalaemia, hypercalcaemia, disordered citrate metabolism and other tubular dysfunctions following human renal transplantation. Q J Med 1969; 38: 231–254[ISI][Medline]
  3. Better OS, Chaimowitz C, Naveh Y etal. Syndrome of incomplete renal tubular acidosis after cadaver kidney transplantation. Ann Intern Med 1969; 71: 39–46[ISI][Medline]
  4. Mookerjee B, Gault MH, Dossetor JB. Hyperchloremic acidosis in early diagnosis of renal allograft rejection. Ann Intern Med 1969; 71: 47–58[ISI][Medline]
  5. Better OS, Chaimowitz C, Alroy GG, Sisman I. Spontaneous remission of the defect in urinary acidification after cadaver kidney homotransplantation. Lancet 1970; 1: 110–112[ISI][Medline]
  6. Liebau G, Müller R, Schad H, Edel HH. Proximal tubuläre Azidose bei nierentransplantierten Patienten. Klin Wochenschr 1970; 48: 624–629[CrossRef][ISI][Medline]
  7. Ladefoged J. Tubular reabsorption of bicarbonate in transplanted cadaver kidneys. Nephron 1973; 10: 212–16
  8. Wilson DR, Siddiqui AA. Renal tubular acidosis after kidney transplantation. Natural history and significance. Ann Intern Med 1973; 79: 352–361[ISI][Medline]
  9. Batlle DC, Mozes MF, Manaligod J, Arruda JA, Kurtzman NA. The pathogenesis of hyperchloremic metabolic acidosis associated with kidney transplantation. Am J Med 1981; 70: 786–796[CrossRef][ISI][Medline]
  10. Jordan M, Cohen EP, Roza A etal. An immunocytochemical study of H+ ATPase in kidney transplant rejection. J Lab Clin Med 1996; 127: 310–314[CrossRef][ISI][Medline]
  11. Heering P, Ivens K, Aker S, Grabensee B. Distal tubular acidosis induced by FK506. Clin Transplant 1998; 12: 465–471[ISI][Medline]
  12. Bank N, Aynediian HS. A micropuncture study of the effect of parathyroid hormone on renal bicarbonate reabsorption. J Clin Invest 1976; 58: 336–344[ISI][Medline]
  13. Better OS. Tubular dysfunction following kidney transplantation. Nephron 1980; 25: 209–213[ISI][Medline]
  14. Rodriguez Soriano J. Renal tubular acidosis: the clinical entity. J Am Soc Nephrol 2002; 13: 2160–2170[Free Full Text]
  15. Widmer B, Gerhardt RE, Harrington JT, Cohen JJ. Serum electrolyte and acid–base composition. The influence of graded degrees of chronic renal failure. Arch Int Med 1979; 139: 1099–1102[Abstract]
  16. Joo KW, Jeon US, Han JS etal. Absence of H+-ATPase in the intercalated cells of renal tissue in classic renal tubular acidosis. Clin Nephrol 1998; 49: 226–231[ISI][Medline]
  17. Penney MD, Oleesky DA. Renal tubular acidosis. Ann Clin Biochem 1999; 36: 408–422[Medline]
  18. Cohen EP, Bastani B, Cohen MR, Kolner S, Hemken P, Gluck SL. Absence of H+-ATPase in cortical collecting tubules of a patient with Sjögren's syndrome and distal renal tubular acidosis. J Am Soc Nephrol 1992; 3: 264–271[Abstract]
  19. DeFranco PE, Haragsim L, Schmitz PG, Bastani B. Absence of vacuolar H+-ATPase pump in the collecting duct of a patient with hypokalemic distal renal tubular acidosis and Sjögren's syndrome. J Am Soc Nephrol 1995; 6: 295–301[Abstract]
  20. Konishi K, Hayashi M, Saruta T. Renal tubular acidosis with autoantibody directed to renal collecting-duct cells. N Engl J Med 1994; 331: 1593–1594[Free Full Text]
  21. Kim S, Lee JW, Park J, Na KY, Joo KW, Ahn C. The urine-blood PCO gradient as a diagnostic index of H(+)-ATPase defect distal renal tubular acidosis. Kidney Int 2004; 66: 761–767[CrossRef][ISI][Medline]
  22. Batlle D, Grupp M, Gaviria M, Kurtzman NA. Distal renal tubular acidosis with intact capacity to lower urinary pH. Am J Med 1982; 72: 751–758[CrossRef][ISI][Medline]
  23. Montalban C, de Francisco AL, Marinoso ML etal. Bone disease in long-term adult kidney transplant patients with normal renal function. Kidney Int 2003; 63: S129–S132
  24. Langman CB, Bushinsky DA, Favus MJ, Coe FL. Ca and P regulation of 1,25(OH)2D3 synthesis by vitamin D-replete rat tubules during acidosis. Am J Physiol 1986; 251: F911–F918
  25. Graham KA, Hoenich NA, Tarbit M, Ward MK, Goodship TH. Correction of acidosis in hemodialysis patients increases the sensitivity of the parathyroid glands to calcium. J Am Soc Nephrol 1997; 8: 627–631[Abstract]
  26. Kraut JA, Kurtz I. Metabolic acidosis of CKD: diagnosis, clinical characteristics, and treatment. Am J Kidney Dis 2005; 6: 978–993
  27. Batlle DC, Gutterman C, Tarka J, Prasad R. Effect of short-term cyclosporine A administration on urinary acidification. Clin Nephrol 1986; 25: S62–S69
  28. Aguilera S, Deray G, Desjobert H, Benhmida M, Le Hoang P, Jacobs C. Effects of cyclosporine on tubular acidification function in patients with idiopathic uveitis. Am J Nephrol 1992; 12: 425–430[ISI][Medline]
  29. Heering P, Grabensee B. Influence of ciclosporin A on renal tubular function after kidney transplantation. Nephron 1991; 59: 66–70[ISI][Medline]
  30. Watanabe S, Tsuruoka S, Vijayakumar S etal. Cyclosporin A produces distal renal tubular acidosis by blocking peptidyl prolyl cis-trans isomerase activity of cyclophilin. Am J Physiol Renal Physiol 2005; 288: F40–F47[Abstract/Free Full Text]
Received for publication: 23. 1.06
Accepted in revised form: 24. 3.06


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 Nephrol Dial TransplantHome page
C. Mitterbauer, G. Heinze, A. Kainz, R. Kramar, W. H. Horl, and R. Oberbauer
ACE-inhibitor or AT2-antagonist therapy of renal transplant recipients is associated with an increase in serum potassium concentrations
Nephrol. Dial. Transplant., May 1, 2008; 23(5): 1742 - 1746.
[Abstract] [Full Text] [PDF]

Home page
 Nephrol Dial TransplantHome page
A. P. Sharma, R. K. Sharma, R. Kapoor, A. Kornecki, S. Sural, and G. Filler
Incomplete distal renal tubular acidosis affects growth in children
Nephrol. Dial. Transplant., October 1, 2007; 22(10): 2879 - 2885.
[Abstract] [Full Text] [PDF]

This Article
Right arrow Abstract Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow All Versions of this Article:
21/9/2615    most recent
gfl211v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (6)
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Schwarz, C.
Right arrow Articles by Haas, M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Schwarz, C.
Right arrow Articles by Haas, M.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?