Division of Cardiology, Respiratory Medicine and Nephrology, Hirosaki University Graduate School of Medicine, Hirosaki, Japan.
Semin Nephrol. 2011 Sep;31(5):453-8. doi: 10.1016/j.semnephrol.2011.08.010.
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.
几十年来，人们已经知道尿酸通过管内晶体沉淀和阻塞肾小管导致急性肾损伤。尿酸晶体在包括痛风性关节炎在内的许多疾病条件下刺激炎症和引发免疫反应。最近，有报道称可溶性尿酸通过非晶体依赖机制刺激血管平滑肌细胞增殖、抑制内皮功能、引起肾血管收缩、损害肾血流自身调节，并诱导炎症反应。本文探讨了尿酸在急性肾损伤中的作用变化。
