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Hyperkalaemia in cyclosporin-treated renal allograft recipients

D Adu, J Turney, J Michael

    Lancet (London, England)
    |August 13, 1983
    PubMed

    Insights

    Cyclosporine treatment in kidney transplant patients can lead to sustained hyperkalemia and acidosis. This is often caused by impaired aldosterone and renin function, worsened by beta-blockers.

    Area of Science:

    • Nephrology
    • Immunosuppression Pharmacology

    Background:

    • Cyclosporine is a common immunosuppressant after renal transplantation.
    • Hyperkalemia is a potential side effect of immunosuppressive therapy.

    Purpose of the Study:

    • To investigate the causes of sustained hyperkalemia in renal allograft recipients treated with cyclosporine.
    • To identify factors contributing to hyperkalemia and associated metabolic acidosis.

    Main Methods:

    • Compared serum potassium levels in cyclosporine recipients versus prednisolone and azathioprine recipients.
    • Analyzed renal function, acid-base status, and hormonal levels (aldosterone, renin) in hyperkalemic patients.
    • Assessed urine pH and the impact of beta-blockers and nephrectomy.

    Main Results:

    • Significantly higher mean serum potassium levels observed in cyclosporine group for 9 months.
    • Seven of 43 cyclosporine patients developed sustained hyperkalemia (6.0-7.1 mmol/l) with hyperchloremic acidosis.
    • Hypoaldosteronism, renal tubular defects, and hyporeninemia (potentially due to beta-blockers) were implicated in hyperkalemic patients.

    Conclusions:

    • Cyclosporine-induced hyperkalemia in renal transplant recipients is linked to impaired potassium and hydrogen ion secretion.
    • Hyporeninemia and hypoaldosteronism, potentially exacerbated by beta-blockers, contribute to this condition.

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