Selected mechanisms of diuretic-induced electrolyte changes

Abstract

Thiazide diuretic therapy has been associated with several biochemical electrolyte imbalances including potassium loss. The onset, duration and magnitude of potassium excretion can influence decisions concerning drug therapy, particularly in hypertensive patients at risk if they develop diuretic-induced hypokalemia. The potassium depletion seen during the course of antihypertensive therapy with thiazides is brought about by 2 primary mechanisms: the increased delivery of sodium to the distal tubules for sodium-potassium exchange, and the development of secondary hyperaldosteronism, which causes resorption of sodium with a loss of potassium into the urine. The diuresis caused by thiazides is maximal between 8 and 12 hours. However, resultant volume contraction stimulates elevated serum aldosterone levels, which can be present for 24 hours or longer. Therefore, potassium loss may exceed the period of diuresis. Diuretics are effective antihypertensive therapy in many patients with mild hypertension. Potassium-sparing agents can offset potassium imbalance that often occurs with diuretics, and thus, these agents have become an important addition to the physician's treatment armamentarium for appropriate patients.