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J Am Soc Nephrol 17: 165-168, 2006
© 2006 American Society of Nephrology
doi: 10.1681/ASN.2006080909
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Supplement Articles

Uric Acid, the Metabolic Syndrome, and Renal Disease

Pietro Cirillo, Waichi Sato, Sirirat Reungjui, Marcelo Heinig, Michael Gersch, Yuri Sautin, Takahiko Nakagawa and Richard J. Johnson

Division of Nephrology, Hypertension and Transplantation, University of Florida, Gainesville, Florida

Address correspondence to: Dr. Pietro Cirillo, Division of Nephrology, Hypertension and Transplantation, Department of Medicine, University of Florida, PO Box 100224, Gainesville, FL 32608. Phone: 352-846-0274; Fax: 352-392-5465; E-mail: pietro.cirillo{at}medicine.ufl.edu

Metabolic syndrome, characterized by truncal obesity, hypertriglyceridemia, elevated BP, and insulin resistance, is recognized increasingly as a major risk factor for kidney disease and also is a common feature of patients who are on dialysis. One feature that is common to patients with metabolic syndrome is an elevated uric acid. Although often considered to be secondary to hyperinsulinemia, recent evidence supports a primary role for uric acid in mediating this syndrome. Specifically, fructose, which rapidly can cause metabolic syndrome in rats, also raises uric acid, and lowering uric acid in fructose-fed rats prevents features of the metabolic syndrome. Uric acid also can accelerate renal disease in experimental animals and epidemiologically is associated with progressive renal disease in humans. It is proposed that fructose- and purine-rich foods that have in common the raising of uric acid may have a role in the epidemic of metabolic syndrome and renal disease that is occurring throughout the world.




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