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In human blood plasma, the reference range of uric acid is typically 3.4–7.2 mg per 100 mL(200–430 μmol/L) for men, and 2.4–6.1 mg per 100 mL for women (140–360 μmol/L). [34] Uric acid concentrations in blood plasma above and below the normal range are known as, respectively, hyperuricemia and hypouricemia .
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 ...
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.
Uremia is the condition of having high levels of urea in the blood. Urea is one of the primary components of urine.It can be defined as an excess in the blood of amino acid and protein metabolism end products, such as urea and creatinine, which would normally be excreted in the urine.
For example, the liver transforms ammonia (which is poisonous) into urea in fish, amphibians and mammals, and into uric acid in birds and reptiles. Urea is filtered by the kidney into urine or through the gills in fish and tadpoles. Uric acid is paste-like and expelled as a semi-solid waste (the "white" in bird excrements).
Allopurinol is used to reduce urate formation in conditions where urate deposition has already occurred or is predictable. The specific diseases and conditions where it is used include gouty arthritis, skin tophi, kidney stones, idiopathic gout; uric acid lithiasis; acute uric acid nephropathy; neoplastic disease and myeloproliferative disease with high cell turnover rates, in which high urate ...
Acute uric acid nephropathy is caused by deposition of uric acid crystals within the kidney interstitium and tubules, leading to partial or complete obstruction of collecting ducts, renal pelvis, or ureter. This obstruction is usually bilateral, and patients follow the clinical course of acute kidney failure.
However, some evidence suggests against a role for uric acid in the neuropathology of Lesch–Nyhan syndrome: Hyperuricemia associated with classic primary gout, which is caused by low uric acid renal clearance rather than uric acid overproduction, is not associated with neuropathology.