Does heparin affect renal sodium and potassium transport and renal function in patients with chronic glomerulonephritis and initial hyperaldosteronism?
Heparin can induce selective hypoaldosteronism, which may worsen renal function in patients with chronic glomerulonephritis and severe baseline renal impairment.
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.
Кутырина et al. (Thu,) studied this question.