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Uric acid as a mediator of diabetic nephropathy
Journal article   Peer reviewed

Uric acid as a mediator of diabetic nephropathy

Diana I Jalal, David M Maahs, Peter Hovind and Takahiko Nakagawa
Seminars in nephrology, Vol.31(5), pp.459-465
09/2011
DOI: 10.1016/j.semnephrol.2011.08.011
PMCID: PMC3197214
PMID: 22000654

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Abstract

Despite advances in the management of patients with diabetes, diabetic nephropathy (DN) remains the most common cause of end-stage renal disease in the United States and worldwide. Inflammation and endothelial dysfunction appear to play a central role in the onset and the progression of DN. Recent evidence has emerged in the past decade to suggest uric acid is an inflammatory factor and may play a role in endothelial dysfunction. This has lead our group and others to explore the role of uric acid in the onset and progression of DN. In this review, we highlight some of the animal and human studies that implicate uric acid in DN. Based on the evidence we review, we conclude the need for properly planned randomized controlled studies to decrease uric acid levels and assess the impact of such therapy on diabetic kidney disease.
Animals Uric Acid - metabolism Diabetic Nephropathies - etiology Humans Disease Progression Diabetic Nephropathies - mortality Disease Models, Animal

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