高尿酸血症损伤肾小管上皮细胞钠钾泵的机制  

Mechanisms of sodium-potassium pump in renal tubular epithelial cells damaged by hyperuricemia

作　　者：林鑫 杨沿浪[1] 王淼 杨晓明[1] 樊惠 LIN Xin;YANG Yanlang;WANG Miao;YANG Xiaoming;FAN Hui(Department of Renal Medicine,Yijishan Hospital,Wannan Medical College,Wuhu 241001,China)

机构地区：[1]皖南医学院弋矶山医院肾内科,安徽芜湖241001

出　　处：《沈阳医学院学报》2021年第5期486-488,506,共4页Journal of Shenyang Medical College

基　　金：安徽省卫生和计划生育委员会科研计划项目(No.2016QK071)。

摘　　要：高尿酸血症与肾小管损伤密切相关,其致病机制众多,其中血尿酸损伤肾小管上皮细胞Na+-K+-ATPase(NKA)信号转导是导致肾小管上皮细胞损害的重要机制,目前相关研究较少。本文将高尿酸血症对肾小管上皮细胞NKA的损伤机制进行综述,探究高尿酸环境下,尿酸是否通过诱导肾小管上皮细胞的氧化应激,从而诱导线粒体功能障碍,并最终导致肾小管上皮细胞NKA受损,从而进一步影响尿酸的代谢,肾小管损伤和一系列炎症反应。Hyperuricemia is closely related to renal tubular damage,and its pathogenic mechanism is complicated.And the signal transduction of Na+-K+ATPase(NKA)damaged by blood uric acid is an important mechanism of renal tubular epithelial cell damage.This article reviews the mechanism of hyperuricemia on the NKA injury of renal tubular epithelial cells,and explores whether hyperuric acid induces oxidative stress in renal tubular epithelial cells,thereby inducing mitochondrial dysfunction and NKA,which further affects uric acid metabolism,renal tubular injury and a series of inflammatory reactions.

关 键 词：高尿酸血症 慢性肾脏病 氧化应激 钠钾泵 

分 类 号：R696[医药卫生—泌尿科学]