Relationship of Cardiorenal Function to Renin-Aldosterone System in Patients with Valvular Heart Disease

Abstract

Metabolic data obtained during sodium (Na) loading, restriction, and depletion with thiazide were compared in 23 patients with valvular heart disease who had cardiac indices (CI) > and < 2.5 liters/min/m 2 . During Na loading (80 mEq Na for 4 days, followed by 150 mEq for 4 days) patients with CI > 2.5 excreted –3.4% Na load than those with the lowest normal values, whereas those with CI < 2.5 excreted –20.8% ( P < 0.02). All 12 patients with CI > 2.5 responded to Na loss with elevation of plasma renin activity (PRA). In contrast, of the ill patients with CI < 2.5, none of the six on the 10 mEq diet, and only two of five on thiazide, responded with an increase in PRA; the urinary aldosterone values paralleled the PRA responses. The renin-angiotensin-aldosterone system responded to changes in Na balance. The magnitude and direction of the responses were influenced by cardiohemodynamic abnormalities. Aldosterone plays an important role in the Na retention in patients with valvular heart disease by stimulating Na-K exchange in the distal tubules of the kidney.