可溶性尿激酶型纤溶酶原激活物受体与局灶节段性肾小球硬化

Soluble urokinase-type plasminogen activator receptor and focal segmental glomerulosclerosis

局灶节段性肾小球硬化(FSGS)是引起终末期肾病的主要原因之一,足细胞损伤是FSGS发生发展的中心环节。循环因子一直被认为是FSGS的致病因素。近来发现循环中可溶性尿激酶型纤溶酶原激活物受体(suPAR)通过激活足细胞β3整合素引起足细胞损伤、脱落,导致FSGS发生,约2/3的FSGS患者血循环中suPAR升高。本文对suPAR与FSGS发病的关系、suPAR在FSGS患者中的特异性及suPAR在FSGS疗效观察中的作用等进行综述。

Focal segmental glomerulosclerosis （FSGS） is a major cause of end-stage renal disease （ESRD）. And podocyte plays a key role in the development of FSGS. Circulating permeability factor has been considered to be pathogenic for FSGS. Recently, it had found that, by binding to 133 integrin on podocytes, suPAR （ soluble urokinase-type plasminogen activator receptor） induced podocyte foot process effacement, proteinuria and initiation of FSGS. Furthermore, high concentration of serum suPAR had been confirmed in approximately two-thirds of patients with FSGS. Here, we will review the role and specificity of suPAR in primary FSGS, and the role of suPAR in clinical practice of FSGS.