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Uric acid is a normal waste product made by the body, but in some people, it can accumulate at higher levels and lead to gout. Gout can be divided into four stages: Hyperuricemia.
Hyperuricosuria is a medical term referring to the presence of excessive amounts of uric acid in the urine. For men this is at a rate greater than 800 mg/day, and for women, 750 mg/day. [1] Notable direct causes of hyperuricosuria are dissolution of uric acid crystals in the kidneys or urinary bladder, and hyperuricemia.
Unless high blood levels of uric acid are determined in a clinical laboratory, hyperuricemia may not cause noticeable symptoms in most people. [5] Development of gout – which is a painful, short-term disorder – is the most common consequence of hyperuricemia, which causes deposition of uric acid crystals usually in joints of the extremities, but may also induce formation of kidney stones ...
An evolutionary loss of urate oxidase (uricase), which breaks down uric acid, in humans and higher primates has made this condition common. [5] The triggers for precipitation of uric acid are not well understood. While it may crystallize at normal levels, it is more likely to do so as levels increase.
Uricosurics are often used in the treatment of gout, a disease in which uric acid crystals form deposits in the joints. By decreasing plasma uric acid levels, help dissolve these crystals, while limiting the formation of new ones. However, the increased uric acid levels in urine can contribute to kidney stones.
Uric acid displays lactam–lactim tautomerism. [4] Uric acid crystallizes in the lactam form, [5] with computational chemistry also indicating that tautomer to be the most stable. [6] Uric acid is a diprotic acid with pK a1 = 5.4 and pK a2 = 10.3. [7] At physiological pH, urate predominates in solution. [medical citation needed]
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