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.