Suppression of plasma renin activity by cyclosporine

John P. Bantle, Robert J. Boudreau, Thomas F. Ferris

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Cyclosporine treatment is associated with hypertension and suppression of plasma renin activity, the causes of which are unclear. To determine whether suppressed plasma renin activity is due to extracellular fluid volume expansion, 10 cyclosporine-treated renal transplant recipients were compared with 10 azathioprine-treated renal transplant recipients and seven patients with renal insufficiency. Glomerular filtration rate and effective renal plasma flow were significantly lower in cyclosporine-treated patients than in azathioprine-treated patients. Upright plasma renin activity was suppressed in cyclosporine-treated patients (cyclosporine 2.9 ± 0.9, azathioprine 4.7 ± 0.9, renal insufficiency 5.2 ± 1.9 ng/ml/hour) but could be stimulated by a four-day period of dietary sodium restriction and diuretic administration (cyclosporine) 15.8 ± 4.4 ng/ml/hour). Extracellular fluid volume tended to be higher in cyclosporine-treated patients (cyclosporine 30.7 ± 2.3, azathioprine 26.7 ± 2.5, renal insufficiency 25.5 ± 1.4 percent lean body mass), although the difference between cyclosporine-treated and azathioprine-treated patients did not attain statistical significance. There were no differences in the urinary excretion of prostaglandin E2 or 6-keto prostaglandin F between the two groups of renal transplant recipients. It is concluded that suppression of plasma renin activity by cyclosporine is physiologic and may reflect expansion of extracellular fluid volume, which can be reversed by sodium depletion.

Original languageEnglish (US)
Pages (from-to)59-64
Number of pages6
JournalThe American Journal of Medicine
Issue number1
StatePublished - Jul 1987

Bibliographical note

Funding Information:
From the Department of Medicine and the Division of Nuclear Medicine, University of Minnesota, Minneapolis, Minnesota. This work was supported by Grant HL-17871 and General Clinical Research Center Grant R&400, both from the National Institutes of Health, Bethesda, Maryland, and by a grant-in-aid from Sandoz, Inc., East Hanover, New Jersey. Requests for reprints should be addressed to Dr. John P. Bantle, Box 504 UMHC, University of Minnesota, Minneapolis, Minnesota 55455. Manuscript submitted October 2, 1986, and accepted January 13, 1987.


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