Uric acid is a product of the metabolic breakdown of purine nucleotides, and it is a normal component of urine.

[2] In 1882, the Ukrainian chemist Ivan Horbaczewski first synthesized uric acid by melting urea with glycine.

Xanthine oxidase is a large enzyme whose active site consists of the metal molybdenum bound to sulfur and oxygen.

[10] In general, the water solubility of uric acid and its alkali metal and alkaline earth salts is rather low.

[16] The normal concentration range of uric acid (or hydrogen urate ion) in human blood is 25 to 80 mg/L for men and 15 to 60 mg/L for women[17] (but see below for slightly different values).

[21] In birds and reptiles, and in some desert-dwelling mammals (such as the kangaroo rat), uric acid also is the end product of purine metabolism, but it is excreted in feces as a dry mass.

Such metabolism is anaerobic involving uncharacterized ammonia lyase, peptidase, carbamoyl transferase, and oxidoreductase enzymes.

[24] Radioisotope studies suggest about 1/3 of uric acid is removed in healthy people in their gut with this being roughly 2/3 in those with kidney disease.

[26][27] A proportion of people have mutations in the urate transport proteins responsible for the excretion of uric acid by the kidneys.

[19][31][32] Myogenic hyperuricemia, as a result of the purine nucleotide cycle running when ATP reservoirs in muscle cells are low, is a common pathophysiologic feature of glycogenoses, such as GSD-III, which is a metabolic myopathy impairing the ability of ATP (energy) production for muscle cells.

[33] 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.

[43] Excess blood uric acid (serum urate) can induce gout,[44] a painful condition resulting from needle-like crystals of uric acid termed monosodium urate crystals[45] precipitating in joints, capillaries, skin, and other tissues.

Consumption of large amounts of some types of purine-rich foods, particularly meat and seafood, increases gout risk.

Today, inflammation during attacks is more commonly treated with NSAIDs, colchicine, or corticosteroids, and urate levels are managed with allopurinol.

[54] It is also possible that high levels of uric acid may have a causal role in the development of atherosclerotic cardiovascular disease, but this is controversial and the data are conflicting.

[61] Sevelamer, a drug indicated for prevention of hyperphosphataemia in people with chronic kidney failure, can significantly reduce serum uric acid.