RENIN-ALDOSTERONE SYSTEM CAN RESPOND TO FUROSEMIDE IN PATIENTS WITH HYPERKALEMIC HYPORENINISM

Thirty-four patients (65.3 +/- 3.3 years of age, mean +/- SEM) with hy perkalemia (serum potassium >5.0 mEq/L) had measurement of their renin -aldosterone system. Nineteen patients (56%) had plasma renin activity (PRA) >1.5 ng/mL/h, which was not low, while 15 (44%) had PRA <1.5. T welve of the 15 hyporeninemic hyperkalemic patients were studied to de termine whether their renin-aldosterone system responded to 2 weeks of furosemide, 20 mg daily. Four were nonresponders: PRA averaged 0.3 +/ - 0.1 ng/mL/h, and it did not increase with furosemide or respond to c aptopril before or after furosemide. Eight patients were responders: P RA averaged 0.6 +/- 0.2 ng/mL/h and increased with furosemide to 5.5 /- 3.4 ng/mL/h. Captopril failed to increase PRA before furosemide, bu t PRA increased to 15.3 +/- 8.4 ng/mL/h after furosemide. Plasma aldos terone was low in both nonresponders and responders (3.5 +/- 1.2 ng/dL vs 5.8 +/- 2.5 ng/dL) and did not increase significantly with furosem ide (4.3 +/- 1.7 ng/dl vs 8.7 +/- 2.5 ng/dL). Serum potassium did not fall and therefore did not limit the rise in aldosterone. Renin respon ders had greater body weight, were predominantly female (6/8 vs 2/4) a nd were more likely to have diabetes mellitus (7/8 vs 0/4). Plasma atr ial natriuretic peptide (ANP) fell with furosemide in 8 of 8 responder s and in 1 of the 2 nonresponders in whom it was measured. Neither gro up had suppressed plasma prorenin levels, indicating no suppression of renin gene expression. These results indicate that many hyperkalemic patients do not have suppressed PRA. Further, a majority of patients w ith suppressed PRA have high levels of ANP and can respond to diuretic therapy with a rise in PRA and a fall in ANP, suggesting physiologic suppression of the renin system by volume expansion. A minority of hyp erkalemic patients with suppressed PRA had PRA that did not increase u nder these study conditions.