TY - JOUR
T1 - Effects of Cyclosporine on the Renin-Angiotensin-Aldosterone System and Potassium Excretion in Renal Transplant Recipients
AU - Bantle, John P.
AU - Nath, Karl A.
AU - Sutherland, David E.R.
AU - Najarian, John S.
AU - Ferris, Thomas F.
N1 - Copyright:
Copyright 2015 Elsevier B.V., All rights reserved.
PY - 1985/3
Y1 - 1985/3
N2 - • 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 plasma renin activity and a tubular insensitivity to aldosterone, both of which may impair potassium excretion.
AB - • 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 plasma renin activity and a tubular insensitivity to aldosterone, both of which may impair potassium excretion.
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U2 - 10.1001/archinte.1985.00360030153026
DO - 10.1001/archinte.1985.00360030153026
M3 - Article
C2 - 3883934
AN - SCOPUS:84941812905
VL - 145
SP - 505
EP - 508
JO - Archives of internal medicine (Chicago, Ill. : 1908)
JF - Archives of internal medicine (Chicago, Ill. : 1908)
SN - 2168-6106
IS - 3
ER -