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Uric acid excretion is a physiological process involving the elimination of uric acid, the end product of purine metabolism in humans, primarily via the kidneys (about 70%) and to a lesser extent by the gut[1][5][6][8]. Renal handling of uric acid involves glomerular filtration, extensive reabsorption, and secretion, with only 7–12% of filtered uric acid ultimately excreted in urine in adults[3][5]. Key molecular players in uric acid transport include several specific renal urate transporters: URAT1 (SLC22A12), GLUT9 (SLC2A9), OAT1/3/4 (SLC22A6/8/11), ABCG2 (BCRP), NPT1 and NPT4, among others[1][2][6][7]. Some of these, such as URAT1 and GLUT9, mediate reabsorption, while others, like OAT1/3, NPT4 and ABCG2, mediate secretion and excretion. The balance of these transporter activities determines serum uric acid levels; alterations may cause hyperuricemia, increasing risk for gout, nephrolithiasis, and other comorbidities[1][5][6]. Known drugs such as allopurinol and febuxostat reduce uric acid production, but uricosuric agents (e.g., probenecid, lesinurad) act by inhibiting urate reabsorption transporters such as URAT1[8]. However, these drugs do not target "uric acid excretion" as an entity, but rather act through individual molecular targets. This entry ("uric acid excretion") should be replaced with the names of specific urate transporters or enzymes (for example, "Urate transporter 1 (URAT1)" or "Glucose transporter 9 (GLUT9)") when curating molecular target data for structure, pharmacology, or drug action.
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