Abstract
It has been known for decades that uric acid causes acute kidney injury by intratubular crystal precipitation and obstructing the renal tubules. Uric acid crystals stimulate inflammation and elicit immune responses in many disease conditions, including gouty arthritis. More recently, soluble uric acid has been reported to stimulate proliferation of vascular smooth muscle cells, inhibit endothelial function, cause renal vasoconstriction, impair renal blood flow autoregulation, and induce inflammatory response via crystal-independent mechanisms. This article examines the changing role for uric acid in acute kidney injury.
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