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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 ...
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]
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.
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.
Mutations in the gene lead to hyperuricemia.At least 67 disease-causing mutations in this gene have been discovered: [5] Some men have partial (up to 20% less activity of the enzyme) HGPRT deficiency that causes high levels of uric acid in the blood, which leads to the development of gouty arthritis and the formation of uric acid stones in the urinary tract.
Protein toxicity is the effect of the buildup of protein metabolic waste compounds, like urea, uric acid, ammonia, and creatinine.Protein toxicity has many causes, including urea cycle disorders, genetic mutations, excessive protein intake, and insufficient kidney function, such as chronic kidney disease and acute kidney injury.
In these metabolic myopathies, myogenic hyperuricemia is exercise-induced; inosine, hypoxanthine and uric acid increase in plasma after exercise and decrease over hours with rest. [18] Excess AMP (adenosine monophosphate) is converted into uric acid .
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. Thus, use of these drugs is contraindicated in persons already with a high urine concentration of uric acid (hyperuricosuria). In borderline cases ...
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