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Review
. 2013 Aug;13(4):550-9.
doi: 10.1007/s11892-013-0381-0.

Uric acid lowering to prevent kidney function loss in diabetes: the preventing early renal function loss (PERL) allopurinol study

Collaborators, Affiliations
Review

Uric acid lowering to prevent kidney function loss in diabetes: the preventing early renal function loss (PERL) allopurinol study

David M Maahs et al. Curr Diab Rep. 2013 Aug.

Abstract

Diabetic kidney disease causes significant morbidity and mortality among people with type 1 diabetes (T1D). Intensive glucose and blood pressure control have thus far failed to adequately curb this problem and therefore a major need for novel treatment approaches exists. Multiple observations link serum uric acid levels to kidney disease development and progression in diabetes and strongly argue that uric acid lowering should be tested as one such novel intervention. A pilot of such a trial, using allopurinol, is currently being conducted by the Preventing Early Renal Function Loss (PERL) Consortium. Although the PERL trial targets T1D individuals at highest risk of kidney function decline, the use of allopurinol as a renoprotective agent may also be relevant to a larger segment of the population with diabetes. As allopurinol is inexpensive and safe, it could be cost-effective even for relatively low-risk patients, pending the completion of appropriate trials at earlier stages.

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Conflict of interest statement

The authors have no conflicts of interest to disclose.

Disclosure

David M. Maahs declares that he has no conflict of interest.

M. Luiza Caramori declares that she has no conflict of interest.

David Z.I. Cherney declares that he has no conflict of interest.

Andrzej T. Galecki declares that he has no conflict of interest.

Chuanyun Gao declares that she has no conflict of interest.

Diana Jalal has received ASN honoraria for speaking on the role of uric acid in kidney and cardiac disease in the elderly.

Bruce A. Perkins is a Senior Advisory Board Member for Neurometrix Inc.; and has been a Site investigator for a sponsored clinical trial for Medtronic Inc.; a Co-PI for a sponsored clinical trial by Boehringer Ingelheim; and has received speaker honoraria from Medtronic Inc., Roche, GlaxoSmithKline, Johnson & Johnson, Novo Nordisk, and Eli Lilly.

Rodica Pop-Busui declares that she has no conflict of interest.

Peter Rossing serves on the board for Astra Zeneca/BMS, Eli Lilly, Janssen, Novo Nordisk, and Astellas; has received grant support from Novo Nordisk, Novartis, and Abbott; has received payment for lectures including service on speakers bureaus from Astra Zeneca/BMS, Novartis, and Sanofi-Aventis; and has stock/stock options with Novo Nordisk.

Michael Mauer declares that he has no conflict of interest.

Alessandro Doria has received research grant support from Sanofi-Aventis; has received travel/accommodations expenses covered or reimbursed from the American Society of Nephrology and the Italian Society of Diabetology.

Figures

Figure 1
Figure 1
Mechanisms through which increased uric acid may contribute to the development of diabetic nephropathy.

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