Uric Acid as a Mediator of Diabetic Nephropathy

被引：85

作者：

Jalal, Diana I. ^{[1
]}

Maahs, David M. ^{[2
]}

Hovind, Peter ^{[3
,4
]}

Nakagawa, Takahiko ^{[1
]}

机构：

[1] Univ Colorado Denver, Div Renal Dis & Hypertens, Aurora, CO 80045 USA

[2] Univ Colorado Denver, Barbara Davis Ctr Childhood Diabet, Aurora, CO 80045 USA

[3] Glostrup Cty Hosp, Dept Clin Physiol & Nucl Med, Glostrup, Denmark

[4] Steno Diabet Ctr, DK-2820 Gentofte, Denmark

来源：

SEMINARS IN NEPHROLOGY | 2011年 / 31卷 / 05期

基金：

美国国家卫生研究院;

关键词：

Uric acid; diabetes; kidney disease; CHRONIC-KIDNEY-DISEASE; GROWTH-FACTOR-BETA; EXAMINATION SURVEY NHANES; ACTIVATED PROTEIN-KINASE; EVALUATION PROGRAM KEEP; MATRIX GENE-EXPRESSION; BLOOD-PRESSURE; HIGH GLUCOSE; TGF-BETA; MESANGIAL CELLS;

D O I：

10.1016/j.semnephrol.2011.08.011

中图分类号：

R5 [内科学]; R69 [泌尿科学（泌尿生殖系疾病）];

学科分类号：

1002 ; 100201 ;

摘要：

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. Semin Nephrol 31:459-465 Published by Elsevier Inc.

引用

页码：459 / 465

页数：7

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