![]() Persistent acidic urine is the most common cause of uric acid stone formation. These factors are TH acidic urine, dehydration, and hyperuricosuria. In uric acid nephrolithiasis, uric acid is handled by the renal system, and three factors can influence uric acid stone formation. Uric acid levels can be elevated ten to 15 years before clinical manifestations of gout. Gout has a male predominance in a 4:1 ratio of men to women. Precipitation is enhanced in acidic environments and cold environments, leading to increased precipitation in peripheral joints, such as the great toe. When tissues are saturated with urate, crystals will precipitate. This leads to the precipitation of urate monohydrate crystals within a joint. Gout is a metabolic disorder that allows for the accumulation of uric acid in the blood and tissues. This transport can be stimulated by organic acids (lactate and acetoacetate, and beta-hydroxybutyrate), medications (niacin, pyrazinamide, ethambutol, cyclosporin, and chemotherapy) and reduced extracellular fluid volume resulting in hyperuricemia. Proximal tubular reabsorption of uric acid is controlled by URAT1 (uric acid transporter 1). The acute or chronic decrease in glomerular filtration can result in hyperuricemia. Underexcretion appears to be a combination of decreased glomerular filtration, decreased tubular secretion, and enhanced tubular reabsorption. 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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