肾素-血管紧张素系统在糖尿病肾病肾脏足细胞损伤中的作用

Abnormality of Renin-Angiotensin System in Podocyte Dysfunction in Diabetic Kidney Disease

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 kidney disease （DKD） is currently the leading cause of end-stage renal disease （ESRD）. DKD is stamped by proteinuria and progressive renal dysfunction. Excessive activation of RAS under hyperglycemic condition is associated with the development of DKD. Suppression of RAS markedly reduces proteinuria and retards progression of DKD in clinic. Podocyte forms the final barrier to protein in glomerular filtration. Podocyte injury leads to abnormality in glomerular filtration permeability, results in proteinuria. Various components of RAS have been identified to be expressed in podocyte. Here we re- viewed the progress on RAS in regulating the function of podocyte and progress of DKD.