Mechanistic insights of soluble uric acid-related kidney disease

• Published in: Current medicinal chemistry
• Main Authors: Pan, Jing, Shi, Min, Ma, Liang, Fu, Ping
• Format: Journal Article
• Language: English
• Published: United Arab Emirates 01.01.2020
• Subjects: Soluble uric acid; hyperuricemia; kidney injury
• ISSN: 1875-533X
• DOI: 10.2174/0929867326666181211094421

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.