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糖尿病肾病(diabetic kidney disease,DKD)作为诱发终末期肾脏病(end-stage renal disease,ESRD)的主要原因,至今其病理机制仍不十分清楚。DKD病程中蛋白尿持续增多并伴随肾素-血管紧张素系统(renin-angiotensin system,RAS)过度激活。阻断RAS能改善蛋白尿,有良好的临床肾脏保护作用。足细胞表达RAS的各成员,作为肾小球滤过的最后屏障,其损伤与蛋白尿的发生关系密切。本文就RAS与足细胞损伤在DKD病理中作用作一简单综述。
Diabetic nephropathy (DKD), as the main cause of end-stage renal disease (ESRD), remains unclear until now. Proteinuria continues to increase in the course of DKD and is over-activated by the renin-angiotensin system (RAS). Blockade of RAS can improve proteinuria, have a good clinical protection of the kidneys. Each member of podocytes expressing RAS, as the last barrier of glomerular filtration, has a close relationship with the occurrence of proteinuria. This article briefly reviews the role of RAS and podocyte injury in the pathology of DKD.