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REVIEW
Membrane Biology Program and Renal Division, Brigham and Women’s Hospital and Harvard Medical School, Boston, Massachusetts
Division of Nephrology, Hypertension, and Transplantation, University of Florida, Gainesville, Florida
Department of Nephrology, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan
Department of Pharmacology and Toxicology, Kyorin University School of Medicine, Tokyo, Japan
mhediger{at}rics.bwh.harvard.edu
Humans excrete uric acid as the final breakdown product of unwanted purine nucleotides. Urate scavenges potential harmful radicals in our body. However, in conjunction with genetic or environmental (especially dietary) factors, urate may cause gout, nephrolitiasis, hypertension, and vascular disease. Blood levels of urate are maintained by the balance between generation and excretion. Excretion requires specialized transporters located in renal proximal tubule cells, intestinal epithelial cells, and vascular smooth muscle cells. The recently identified human urate transporters URAT1, MRP4, OAT1, and OAT3 are thought to play central roles in homeostasis and may prove interesting targets for future drug development.
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