Summary scheme of the pathways to produce uric acid, to convert it into allantoin by the liver enzyme uricase, and to excrete it. It has antioxidant properties that may be protective but can also be pro-oxidant, depending on its chemical microenvironment. The balance between these pathways regulates blood urate concentrations, which are higher in humans and apes due to inactivation of the uricase genes.

Hyperuricemia predisposes to disease through the formation of urate crystals that cause gout, but hyperuricemia, independent of crystal formation, has also been linked with hypertension, atherosclerosis, insulin resistance, and diabetes. Hyperuricemia can lead to gout and possibly to cardiovascular effects, whereas hyperuricosuria may leads to uric acid crystal–induced pathologies.
We also cover the genetics of urate transport, including URAT1, and recent studies identifying SLC2A9, which encodes the glucose transporter family isoform Glut9, as a major determinant of plasma uric acid levels and of gout development.

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