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Review
. 2020 Jun 26:2020:5817348.
doi: 10.1155/2020/5817348. eCollection 2020.

Research Advances in the Mechanisms of Hyperuricemia-Induced Renal Injury

Hong-Yong Su  1 , Chen Yang  1 , Dong Liang  1 , Hua-Feng Liu  1
Affiliations
Review

Research Advances in the Mechanisms of Hyperuricemia-Induced Renal Injury

Hong-Yong Su et al. Biomed Res Int. .

Abstract

Uric acid is the end product of purine metabolism in humans, and its excessive accumulation leads to hyperuricemia and urate crystal deposition in tissues including joints and kidneys. Hyperuricemia is considered an independent risk factor for cardiovascular and renal diseases. Although the symptoms of hyperuricemia-induced renal injury have long been known, the pathophysiological molecular mechanisms are not completely understood. In this review, we focus on the research advances in the mechanisms of hyperuricemia-caused renal injury, primarily on oxidative stress, endothelial dysfunction, renal fibrosis, and inflammation. Furthermore, we discuss the progress in hyperuricemia management.

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Conflict of interest statement

The authors declare that they have no conflicts of interest to disclose.

Figures

Figure 1
Figure 1
Mechanisms of hyperuricemia-induced renal injury. UA: uric acid; SUA: soluble uric acid; MSU: monosodium urate; ROS: reactive oxygen species; RAS; renin-angiotensin system; ET-1: endothelin 1; NO: nitric oxide; EndoMT: endothelial-to-mesenchymal transition; EMT: epithelial-to-mesenchymal transition; MMP: matrix metalloproteinase; ER stress: endoplasmic reticulum stress.
See this image and copyright information in PMC

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