Division of Nephrology, University of Michigan Medical School, Ann Arbor, 48109, USA.
Adv Chronic Kidney Dis. 2011 Jul;18(4):233-42. doi: 10.1053/j.ackd.2011.06.001.
Protein leak in the urine is a harbinger of disruption of the glomerular filtration barrier. It also correlates with disease progression and development of ESRD. At present, therapies are aimed at decreasing proteinuria to decrease further damage to the filter and as a marker of remission. Understanding the mechanism of molecular events that lead to protein leak is vital to developing new therapeutic interventions. There has been tremendous progress over the last decade in identifying gene defects which result in hereditary proteinuric defects. This has led to identifying pathways by which these genes regulate the structure and function of the components of the filtration barrier, namely the podocytes, mesangial cells, endothelial cells, and the basement membrane. Using gene knockout mouse models, a role of tubular cells in regulating proteinuria is also emerging. In this review, we have attempted to present some of the prevailing understanding of the underlying mechanisms and physiology of proteinuria.
尿蛋白渗漏是肾小球滤过屏障破坏的先兆。它也与疾病进展和 ESRD 的发展相关。目前,治疗方法旨在减少蛋白尿,以减少对滤器的进一步损害,并作为缓解的标志物。了解导致蛋白渗漏的分子事件的机制对于开发新的治疗干预措施至关重要。在过去十年中,在确定导致遗传性蛋白尿缺陷的基因缺陷方面取得了巨大进展。这导致确定了这些基因调节滤过屏障成分(即足细胞、系膜细胞、内皮细胞和基底膜)的结构和功能的途径。使用基因敲除小鼠模型,肾小管细胞在调节蛋白尿中的作用也正在显现。在这篇综述中,我们试图介绍对蛋白尿的潜在机制和生理学的一些现有理解。