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Does Altered Uric Acid Metabolism Contribute to Diabetic Kidney Disease Pathophysiology?

  • Microvascular Complications—Nephropathy (M Afkarian and B Roshanravan, Section Editors)
  • Published:
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Abstract

Purpose of Review

Multiple experimental and clinical studies have identified pathways by which uric acid may facilitate the development and progression of chronic kidney disease (CKD) in people with diabetes. However, it remains uncertain if the association of uric acid with CKD represents a pathogenic effect or merely reflects renal impairment.

Recent Findings

In contrast to many published reports, a recent Mendelian randomization study did not identify a causal link between uric acid and CKD in people with type 1 diabetes. Two recent multicenter randomized control trials, Preventing Early Renal Function Loss in Diabetes (PERL) and FEbuxostat versus placebo rAndomized controlled Trial regarding reduced renal function in patients with Hyperuricemia complicated by chRonic kidney disease stage 3 (FEATHER), were recently designed to assess if uric acid lowering slows progression of CKD.

Summary

We review the evidence supporting a role for uric acid in the pathogenesis of CKD in people with diabetes and the putative benefits of uric acid lowering.

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Acknowledgments

We would like to thank Ms. Leslie Firkins and Ms. Serena Cumber for their help in preparation of this manuscript. The content is solely the responsibility of the authors and does not necessarily represent the official views of the Dialysis Clinic, Inc.

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Correspondence to Philip Zager.

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Ambreen Gul is an employee of Dialysis Clinic, Inc.

Philip Zager is an employee of the University of New Mexico and Dialysis Clinic, Inc.

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This article does not contain any studies with human or animal subjects performed by any of the authors.

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This article is part of the Topical Collection on Microvascular Complications—Nephropathy

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Gul, A., Zager, P. Does Altered Uric Acid Metabolism Contribute to Diabetic Kidney Disease Pathophysiology?. Curr Diab Rep 18, 18 (2018). https://doi.org/10.1007/s11892-018-0985-5

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