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The picture of acute kidney failure is observed: decreased urine production and rapidly rising serum creatinine levels. Acute uric acid nephropathy is differentiated from other forms of acute kidney failure by the finding of a urine uric acid/creatinine ratio > 1 in a random urine sample.
Although foods such as meat and seafood can elevate serum urate levels, genetic variation is a much greater contributor to high serum urate. [ 26 ] [ 27 ] A proportion of people have mutations in the urate transport proteins responsible for the excretion of uric acid by the kidneys.
Unless high blood levels of uric acid are determined in a clinical laboratory, hyperuricemia may not cause noticeable symptoms in most people. [4] 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 ...
Hypouricemia or hypouricaemia is a level of uric acid in blood serum that is below normal. In humans, the normal range of this blood component has a lower threshold set variously in the range of 2 mg/dL to 4 mg/dL, while the upper threshold is 530 μmol/L (6 mg/dL) for women and 619 μmol/L (7 mg/dL) for men. [1]
In general, uricosuric drugs act on the proximal tubules in the kidneys, where they interfere with the absorption of uric acid from the kidney back into the blood. Several uricosurics are known to act in vitro by blocking the function of a protein encoded by the gene SLC22A12, also known as urate transporter 1 or URAT1. URAT1 is the central ...
Gout is due to persistently elevated levels of uric acid (urate) in the blood (hyperuricemia). [2] [5] This occurs from a combination of diet, other health problems, and genetic factors. [1] [2] At high levels, uric acid crystallizes and the crystals deposit in joints, tendons, and surrounding tissues, resulting in an attack of gout. [1]