Uric acid as a mediator of diabetic nephropathy

Semin Nephrol. 2011 Sep;31(5):459-65. doi: 10.1016/j.semnephrol.2011.08.011.


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.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, U.S. Gov't, Non-P.H.S.
  • Review

MeSH terms

  • Animals
  • Diabetic Nephropathies / etiology*
  • Diabetic Nephropathies / mortality
  • Disease Models, Animal
  • Disease Progression
  • Humans
  • Uric Acid / metabolism*


  • Uric Acid