![]() Urate excretion occurs primarily in the kidneys and is responsible for hyperuricemia in 90% of individuals. Conditions of accelerated cell breakdown or turnover such as rhabdomyolysis, hemolysis, and tumor lysis, can also be a purine source and, thus, increase urate production. Endogenous production of the purine production can be accelerated by phosphoribosylpyrophosphate (PRPP) synthetase activity as well as a defect in the regulatory enzyme hypoxanthine phosphoribosyltransferase (HPRT). Beer, which is purine-rich, also increases uric acid levels by decreasing kidney excretion. Foods rich in purine include all meats but specifically organ meats (kidneys, liver, “sweet bread”), game meats, and some seafood (anchovies, herring, scallops). Urate production is accelerated by purine-rich diets, endogenous purine production, and high cell breakdown, and it is responsible for a minority of cases of hyperuricemia. This enzyme converts urate to the more water-soluble form of allantoin. Other mammals have lower uric acid levels due to the activity of uricase. In the kidneys, it is filtered and secreted, and 90% is reabsorbed. About two-thirds of uric acid is excreted in the kidneys, and a third is excreted into the intestine. Purine metabolism mainly occurs in the liver, but it can also be produced in any other tissue that contains xanthine oxidase (intestines). At the normal physiological pH of 7.4, uric acid circulates in the ionized form of urate. Uric acid (2,6,8 trioxypurine-C5H4N4O3) is the result of purine breakdown.
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