Glucose-induced paradoxical hyperkalemia in patients with suppression of the renin-aldosterone system: prevention by sodium depletion.

A paradoxical transitory elevation of serum potassium concentration after intravenous infusion of hypertonic glucose has been found in 6 renal and/or hypertensive patients with suppression of the renin-aldosterone system (RAS) while on high sodium intake. Sodium restriction induced a dramatic increase in plasma renin activity (PRA) and/or plasma aldosterone (PA) in every patient, a substantial fall in the elevated serum potassium levels in 4 out of the 6 patients and a marked increase in fractional potassium excretion. During sodium restriction the glucose-induced paradoxical transitory hyperkalemia was abolished. The study confirmed the important extrarenal influence of aldosterone in the maintenance of normal potassium level in the hyperosmolal extracellular fluid and showed that: i) high sodium intake may predispose to hazardous hyperkalemia after massive glucose loading in certain nondiabetic patients with liability to suppression of aldosterone; ii) sodium restriction abolishes the glucose-induced abnormal serum potassium response.