This article is part of the supplement: Gout and Hyperuricemia
Recent developments in our understanding of the renal basis of hyperuricemia and the development of novel antihyperuricemic therapeutics
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
Citation and License
Arthritis Research & Therapy 2006, 8(Suppl 1):S4 doi:10.1186/ar1909Published: 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.