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Current Medicinal Chemistry

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ISSN (Online): 1875-533X

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Review Article

Mechanistic Insights of Soluble Uric Acid-related Kidney Disease

Author(s): Pan Jing, Min Shi, Liang Ma* and Ping Fu*

Volume 27, Issue 30, 2020

Page: [5056 - 5066] Pages: 11

DOI: 10.2174/0929867326666181211094421

Price: $65

Abstract

Hyperuricemia, defined as the presence of elevated serum uric acid (sUA), could lead to urate deposit in joints, tendons, kidney and other tissues. Hyperuricemia as an independent risk factor was common in patients during the causation and progression of kidney disease. Uric acid is a soluble final product of endogenous and dietary purine metabolism, which is freely filtered in kidney glomeruli where approximately 90% of filtered uric acid is reabsorbed. Considerable studies have demonstrated that soluble uric acid was involved in the pathophysiology of renal arteriolopathy, tubule injury, tubulointerstitial fibrosis, as well as glomerular hypertrophy and glomerulosclerosis. In the review, we summarized the mechanistic insights of soluble uric acid related renal diseases.

Keywords: Soluble uric acid, hyperuricemia, kidney injury, Uric acid (UA), renal arteriolopathy, uric acid-induced kidney injury.

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