Abstract
Intracellular citrate is a central component of the tricarboxylic acid cycle; its excretion in the urine was utilized by Krebs and coworkers to demonstrate this biochemical pathway in whole animals. Subsequently, urinary citrate has been viewed as a window on renal metabolism [1]. Additionally, renal physiologists and biochemists have been intrigued for decades by the dramatic changes in urinary citrate which occur with changes in acid-base homeostasis. In recent years, renal handling of citrate and citrate excretion in the urine have attracted renewed interest because of several considerations. First, modern techniques in renal physiology (such as, transport studies in brush border membrane vesicles and perfused proximal tubules) have provided insights into the cellular and molecular mechanisms of citrate transport [2]. Also, excretion of urinary citrate (and other organic anions) has been recognized to influence systemic acid-base status, at least in certain species [3]. And perhaps most importantly, urinary citrate has been increasingly recognized as an important endogenous inhibitor of calcium nephrolithiasis [4]. This review will focus on the renal handling of citrate, particularly the mechanisms of citrate transport in the proximal tubule, and briefly discuss other aspects of citrate metabolism.
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