Contrasting Effects of Various Potassium Salts on Acid-Base Status, Urinary Citrate Excretion, and Renal Citrate Clearance

Abstract

Recently, we have demonstrated that hypocitraturia is a common finding in patients with nephrolithiasis (1). Oral potassium citrate (K-Citrate) treatment has been effective in enhancing renal citrate excretion in such patients (2). The citraturic action of potassium citrate is believed to be the result of the alkali load provided, affecting the renal handling of citrate (2). However, there are data indicating that renal citrate metabolism is affected by bicarbonate ions separate from any action on blood pH (3). Potassium may also play a role in controlling renal citrate excretion since hypokalemia decreases urinary citrate excretion (4). Moreover, despite suggestions to the contrary, orally-administered citrate may theoretically increase urinary citrate by escaping metabolic degradation in vivo and appearing directly in the urine. This study was done in order to determine which of the above factors are responsible for the citraturic action of potassium citrate.