Department of Medicine, Miller School of Medicine, University of Miami, Miami, Florida 33136, USA.
Curr Opin Nephrol Hypertens. 2012 Jul;21(4):428-32. doi: 10.1097/MNH.0b013e328354a681.
We discuss recent work on the pathogenetic mechanism of focal segmental glomerulosclerosis (FSGS) and its relationship to soluble urokinase receptor (suPAR).
Primary FSGS can affect both children and adults. The disease can recur after kidney transplantation suggesting the involvement of a causative circulating factor. Recent work suggests that approximately two-thirds of FSGS patients have elevated levels of serum suPAR, which confers risk to both native and posttransplant FSGS.
Future studies that are geared to understand the clinical implications of high suPAR levels in native FSGS as well as in the pretransplant and posttransplant setting will allow for better patient risk stratification and more targeted treatment options.
我们讨论了局灶节段性肾小球硬化症(FSGS)发病机制的最新研究进展及其与可溶性尿激酶型纤溶酶原激活物受体(suPAR)的关系。
原发性 FSGS 可发生于儿童和成人。肾移植后疾病可复发,提示存在致病循环因子。最近的研究表明,大约三分之二的 FSGS 患者血清 suPAR 水平升高,这使原发性和移植后 FSGS 均具有发病风险。
未来的研究旨在了解血清 suPAR 水平升高对原发性 FSGS 以及移植前和移植后患者的临床意义,这将有助于更好地对患者进行风险分层,并提供更有针对性的治疗选择。