Serum Potassium Concentrations in Cyclosporine- and Azathioprine-Treated Renal Transplant Patients

Foley, Richard J.; Hamner, Ronald W.; Weinman, Edward J.

doi:10.1159/000183479

Cited by 27 publications

(13 citation statements)

References 10 publications

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“…Although cyclosporin A (CsA) has been hailed as a major advance in transplantation, increasing both graft and patient survival, its use is sometimes limited by nephrotoxicity and hyperkalemia which have been commonly observed in renal transplant patients successfully treated with cyclosporine (1,2). The pathogenesis of CsA-induced nephrotoxicity remains unclear.…”

Section: Introductionmentioning

confidence: 99%

“…Formerly, several reports have suggested that the development of hyperkalemia is specifically associated with the therapeutic administration of CsA, and it was believed that the mechanism of hyperkalemia involved the reduction of potassium secretion as a result of renal tubular damage and hypoaldosteronism (2,5). But recently, Suzuki et al (6) reported that prolonged use of CsA suppresses DNA and RNA synthesis, as well as Na Thyroxine administration has shown protective effects in several experimental models of acute renal failure induced by various and numerous nephrotoxic agents.…”

Section: Introductionmentioning

confidence: 99%

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Effects of Thyroxine on Hyperkalemia and Renal Cortical Na(+), K(+) - ATPase Activity Induced by Cyclosporin A

et al. 2002

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Cyclosporin A (CsA)-induced hyperkalemia is caused by alterations in transepithelial K+ secretion resulting from the inhibition of renal tubular Na+, K+ -ATPase activity. Thyroxine enhances renal cortical Na+, K+ -ATPase activity. This study investigated the effect of thyroxine on CsA-induced hyperkalemia. Sprague-Dawley rats were treated with either CsA, thyroxine, CsA and thyroxine, or olive-oil vehicle. CsA resulted in an increase in BUN and serum K+, along with a decrease in creatinine clearance, fractional excretion of potassium, and renal cortical Na+, K+ -ATPase activity, as compared with oil vehicle administration. Histochemical study showed reduced Na+, K+ -ATPase activity in the proximal tubular epithelial cells of the CsA-treated compared with the oil-treated rats. Histologically, isometric intracytoplasmic vacuolation, disruption of the arrangement and swelling of the mitochondria, and a large number of lysosomes in the tubular epithelium were characteristic of the CsA-treated rats. Co-administration of thyroxine prevented CsA-induced hyperkalemia and reduced creatinine clearance, Na+, K+ -ATPase activity, and severity of the histologic changes in the renal tubular cells when compared with the CsA-treated rats. Thyroxine increased the fractional excretion of potassium via the preservation of Na+, K+ -ATPase activity in the renal tubular cells. Thus, the beneficial effects of thyroxine may be suited to treatment modalities for CsA-induced hyperkalemia.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Effects of Thyroxine on Hyperkalemia and Renal Cortical Na(+), K(+) - ATPase Activity Induced by Cyclosporin A

et al. 2002

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“…In order to check this hypothesis, we studied the use of the drug in two clinical situations : in kidney transplantation and in patients with steroid-resistant idiopathic nephrotic syndrome. In neither of these two groups did we detect hyperkalaemia, which is considered as one of the sideeffects of the drug [26,27]. Although a high level of blood potassium was found in the transplant patients before surgery, it decreased to normokalaemia immediately after transplantation.…”

Section: Discussionmentioning

confidence: 65%

Lack of effect of clinical doses of cyclosporin A on erythrocyte Na+/K+-ATPase activity

FERRER-MARTÍNEZ¹,

Felipe²,

BARCELÓ³

et al. 1999

Clinical Science

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Cyclosporin A (CsA) may exert its cytotoxic effects by altering the activity of different plasma membrane transport systems. Although CsA may act at the gene level, it has been also suggested that it can directly alter transport processes at the plasma membrane. To examine this possibility in a physiological context, we determined Na(+)/K(+)-ATPase activity in erythrocytes from two groups of subjects receiving CsA treatment: group I consisted of kidney transplant patients, and group II comprised patients with steroid-resistant idiopathic nephrotic syndrome. Group I patients showed a marked decrease (35%) in the activity of the Na(+)/K(+)-ATPase in erythrocytes immediately after surgery, before the initiation of CsA treatment. The activity remained low 2 days after the introduction of CsA, but had recovered to the original (pre-surgery) value 1 month later. Group II patients showed the same pattern of erythrocyte Na(+)/K(+)-ATPase activity as those in group I. When the blood CsA levels from all patients were plotted against the corresponding erythrocyte Na(+)/K(+)-ATPase transport activity, a significant linear correlation was found. Higher levels of CsA in the blood were correlated significantly with increased Na(+)/K(+)-ATPase activities. The blood sodium concentration was also correlated positively with both erythrocyte Na(+)/K(+)-ATPase activity and blood CsA concentration. Thus CsA treatment is not associated with inhibition of the Na(+)/K(+)-ATPase in erythrocytes.

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“…An early description of these effects was published in 1983 when seven out of 43 patients treated with cyclosporine (CsA) treated developed hyperkalemia and hyperchloremic metabolic acidosis despite a preserved glomerular filtration rate (1). Subsequently, other studies have reported an incidence of CNI-associated hyperkalemia and hypertension that ranges between 10% and 33% (2)(3)(4), and which appears to be higher with tacrolimus.…”

Section: Case Discussionmentioning

confidence: 95%

American Society of Nephrology Quiz and Questionnaire 2015

Rosner

Perazella

Choi

2016

Clinical Journal of the American Society of Nephrology

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The Nephrology Quiz and Questionnaire remains an extremely popular session for attendees of the annual Kidney Week meeting of the American Society of Nephrology. During the 2015 meeting the conference hall was once again overflowing with eager quiz participants. Topics covered by the experts included electrolyte and acid-base disorders, glomerular disease, end-stage renal disease and dialysis, and kidney transplantation. Complex cases representing each of these categories together with single-best-answer questions were prepared and submitted by the panel of experts. Before the meeting, training program directors of nephrology fellowship programs and nephrology fellows in the United States answered the questions through an internet-based questionnaire. During the live session members of the audience tested their knowledge and judgment on the same series of case-oriented questions in a quiz. The audience compared their answers in real time using a cell-phone app containing the answers of the nephrology fellows and training program directors. The results of the online questionnaire were displayed, and then the quiz answers were discussed. As always, the audience, lecturers, and moderators enjoyed this highly educational session. This article recapitulates the session and reproduces selected content of educational value for the Clinical Journal of the American Society of Nephrology readers. Enjoy the clinical cases and expert discussions.

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Serum Potassium Concentrations in Cyclosporine- and Azathioprine-Treated Renal Transplant Patients

Cited by 27 publications

References 10 publications

Effects of Thyroxine on Hyperkalemia and Renal Cortical Na(+), K(+) - ATPase Activity Induced by Cyclosporin A

Effects of Thyroxine on Hyperkalemia and Renal Cortical Na(+), K(+) - ATPase Activity Induced by Cyclosporin A

Lack of effect of clinical doses of cyclosporin A on erythrocyte Na+/K+-ATPase activity

American Society of Nephrology Quiz and Questionnaire 2015

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