HEPARIN-INDUCED ALDOSTERONE SUPPRESSION AND HYPERKALEMIA

PURPOSE: TO review the effects of heparin and heparinoid compounds on aldosterone physiology and associated induction of hyperkalemia. MATER IALS AND METHODS: A comprehensive literature search (of human and anim al data) was carried out by computer and by using reference citations from primary sources. RESULTS: Heparin and its congeners are predictab le, potent inhibitors of aldosterone production. This inhibitory effec t is specific for the zona glomerulosa; other corticosteroids are not affected. Aldosterone suppression occurs within a few days of initiati on of therapy, is reversible, and is independent of either anticoagula nt effect or route of administration. Decreases in aldosterone levels may occur with heparin dosages as low as 5,000 U BID. The most importa nt, but probably not the only mechanism of aldosterone inhibition appe ars to involve reduction in both the number and affinity of the angiot ensin-ll receptors in the zona glomerulosa. Prolonged use of heparin c auses marked reduction in the width of the adrenal zona glomerulosa. C ONCLUSIONS: Aldosterone suppression results in natriuresis and less pr edictably in decreased excretion of potassium. Greater than normal ser um potassium levels occur in about 7% of patients, but marked hyperkal emia generally requires the presence of additional factors perturbing potassium balance (in particular, renal insufficiency, diabetes mellit us, or the use of certain medications). Heparin-induced increases in s erum potassium need to be better anticipated by clinicians. Serum pota ssium levels should be monitored periodically in patients being given heparin for 3 or more days, and in patients at relatively high risk fo r hyperkalemia, the monitoring interval should probably be no greater than 4 days.