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Renin-Angiotensin-Aldosterone System in Cyclosporin ATreated Renal Allograft Recipients B. Brigitte Stanek J. Josef Kovarik W. Werner Buschbeck K. Karl Silberbauer W. Wulf Pinggera Brigitte Stanek, II. Medizinische Universitätsklinik, Garnisonsgasse 13, A-1090 Wien (Austria) Dear Sir, There is still ongoing debate whether hypertension arising in renal allograft recipients on cyclosporin A (Cy-A) relates to stimulation of the renin-angiotensin-al-dosterone system (RAAS). In animal experiments Cy-A has been demonstrated to enhance renin content and release from renal cortical slices and to increase plasma renin activity (PRA) [1–3]. In contrast, however, low or low-normal PRA was found in 5 of 7 hypertensive patients treated with Cy-A for renal transplantation [4]. We did multiple measurements of PRA and aldoste-rone in 11 Cy-A-treated renal allograft recipients (table I). 10 of 11 patients were hypertensive and successfully treated with labetalol, nifedipine, and dihydralazine. We could not find changes in PRA and aldosterone up to 3 Table I. Plasma renin activity and aldosterone in cyclosporin-treated renal allograft recipients (means ± SEM from 11 patients) Weeks 1 2 3 after transplantation: Plasma renin activity, 0.31 ± 0.05 0.30 ± 0.03 0.32 ± 0.05 ng/ml/h Plasma aldosterone, 114 ± 27 72 ± 18 pg/ml Plasma creatinine, mg/l00 ml Blood pressure, mm Hg weeks after initiation of Cy-A therapy. Although therapy with ß-blockers has to be taken into account, there does not seem to be profound stimulation of basal PRA in our patients shortly after initiation of Cy-A therapy. May be pharmacological stimulation of renin release by inhibiting angiotensin-converting enzyme will give more insight into the activity of the RAAS in renal allograft recipients. This

Renin-Angiotensin-Aldosterone System in Cyclosporin A-Treated Renal Allograft Recipients