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John P. Bantle, MD; Karl A. Nath, MD; David E. R. Sutherland, MD; John S. Najarian, MD; Thomas F. Ferris, MD

Arch Intern Med. 1985;145(3):505-508.

Abstract
• To evaluate the mechanism of cyclosporine-induced hyperkalemia, the renin-angiotensin-aldosterone system and renal potassium clearance were compared in ten renal transplant recipients treated with cyclosporine and treated with azathioprine. After stimulation by a low-sodium diet and furosemide, cyclosporine-treated patients demonstrated lower plasma renin activity when supine (1.9 ±0.3 v 7.8± 1.4 ng/mL/hr) and after standing (0.3±0.7 v 12.2±1.5 ng/ mL/hr). Supine plasma aldosterone levels tended to be lower in cyclosporine-treated patients, (4.8 ±0.8 v 10.5±2.6 ng/dL), although standing plasma aldosterone levels were not different (10.8 ±3.0 v 12.3 ±2.0 ng/dL). After administration of 0.75 mEq of potassium chloride per kilogram of body weight, cyclosporine-treated patients excreted 52%±7.1% of the potassium load in six hours compared with excretion of 67%±7.0% by the azathioprine-treated patients, although there was no difference in plasma aldosterone levels in response to the potassium load in the two groups. These data suggest that cyclosporine causes suppression of

Author Affiliations
From the Departments of Medicine (Drs Bantle, Nath, and Ferris) and Surgery (Drs Sutherland and Najarian), University of Minnesota, Minneapolis.

Footnotes
Accepted for publication Aug 23, 1984.

Reprint requests to Box 91, Mayo Memorial Building, University of Minnesota, Minneapolis, MN 55455 (Dr Bantle).

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