| Literature DB >> 30526453 |
Jing Pan1, Min Shi1, Liang Ma1, Ping Fu1.
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. Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.Entities:
Keywords: Soluble uric acid; Uric acid (UA); hyperuricemia; kidney injury; renal arteriolopathy; uric acid-inducedzzm321990kidney injury
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Year: 2020 PMID: 30526453 DOI: 10.2174/0929867326666181211094421
Source DB: PubMed Journal: Curr Med Chem ISSN: 0929-8673 Impact factor: 4.530