The effects of heparin-induced aldosterone deficiency on renal sodium and potassium transport and renal function were studied in 65 patients with chronic glomerulonephritis and initial hyperaldosteronism. Heparin-induced aldosterone deficiency resulted in increased diuresis, in natriuresis due to decreased sodium reabsorption in the distal nephron, in a fall in serum sodium and an increase in serum potassium concentration. A transient reduction in potassium excretion occurred during the 2-4 days of heparin treatment. In patients with chronic glomerulonephritis and a compromised renin-angiotensin-aldosterone system, heparin may cause drug-induced selective hypoaldosteronism. The suppressive effect of heparin on aldosterone production was partially compensated for by increasing plasma renin activity. Heparin-induced aldosterone deficiency did not change glomerular filtration rate in patients without renal failure. In those with chronic sclerosing glomerulonephritis and a glomerular filtration rate less than 35 ml/min, heparin caused a further decrease in renal function.