Medical implications of hyperuricemia.

Abstract

Uric acid is an oxidation product of purine metabolism, which in primates (in-cluding humans) is largely eliminated by the kidney and the gut. Most non-primate mammals express uricase, an enzyme that converts serum uric acid into allantoin, which is easily excreted by the kidneys. Non-primate mammals thus usually have low serum uric acid (SUA) levels (below 2 mg/ dl), while primates have the potential to develop hyperuricemia, because they lack uricase. In humans, renal under excretion of uric acid is the cause of 90 % of hyperu-ricemia, while 10 % is due to overproduc-tion of uric acid. Uric acid is more toxic to