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Urinary citrate is citric acid excreted in the urine, reflecting the kidney’s handling of citrate filtered and reabsorbed in the proximal tubule. It is a metabolic inhibitor of calcium stone formation, primarily by binding urinary calcium and preventing crystallization into stones[1][2][6][9]. Low urinary excretion (hypocitraturia) is a recognized risk for nephrolithiasis and is influenced by diet, acid-base status, and genetic factors affecting renal citrate transporters such as NaDC1[4][7]. Measurement of urinary citrate is valuable for assessing stone risk and monitoring therapy. Increasing urinary citrate (often via potassium citrate) is an established strategy to prevent stones; hypocitraturia is also linked to risk of bone loss and faster progression of chronic kidney diseases including polycystic kidney disease[1][8]. Urinary citrate is a biochemical analyte, not a molecular therapeutic target.
Urinary alkalinization and increased citrate excretion (Potassium citrate increases urinary pH and citrate levels, inhibiting stone formation by increasing calcium-citrate formation and reducing calcium oxalate supersaturation[1][2][3][5][7])
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