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This article is part of the supplement: Gout and Hyperuricemia

Highly Accessed Open Badges Review

Recent developments in our understanding of the renal basis of hyperuricemia and the development of novel antihyperuricemic therapeutics

Robert Terkeltaub1*, David A Bushinsky2 and Michael A Becker3

Author affiliations

1 San Diego VAMC Rheumatology Section, and University of California San Diego, La Jolla, California, USA

2 University of Rochester School of Medicine, and Nephrology Division, Strong Memorial Hospital, Rochester, New York, USA

3 University of Chicago Pritzker School of Medicine, Chicago, Illinois, USA

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Citation and License

Arthritis Research & Therapy 2006, 8(Suppl 1):S4  doi:10.1186/ar1909

Published: 12 April 2006


Although dietary, genetic, or disease-related excesses in urate production may contribute to hyperuricemia, impaired renal excretion of uric acid is the dominant cause of hyperuricemia in the majority of patients with gout. The aims of this review are to highlight exciting and clinically pertinent advances in our understanding of how uric acid is reabsorbed by the kidney under the regulation of urate transporter (URAT)1 and other recently identified urate transporters; to discuss urate-lowering agents in clinical development; and to summarize the limitations of currently available antihyperuricemic drugs. The use of uricosuric drugs to treat hyperuricemia in patients with gout is limited by prior urolothiasis or renal dysfunction. For this reason, our discussion focuses on the development of the novel xanthine oxidase inhibitor febuxostat and modified recombinant uricase preparations.