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局灶节段性肾小球硬化的发病机制。

The pathogenesis of focal segmental glomerulosclerosis.

作者信息

Jefferson J Ashley, Shankland Stuart J

机构信息

Division of Nephrology, Department of Medicine, University of Washington, Seattle, WA.

Division of Nephrology, Department of Medicine, University of Washington, Seattle, WA.

出版信息

Adv Chronic Kidney Dis. 2014 Sep;21(5):408-16. doi: 10.1053/j.ackd.2014.05.009.

Abstract

Focal segmental glomerulosclerosis (FSGS) is a histologic pattern of injury on kidney biopsy that can arise from a diverse range of causes and mechanisms. Although primary and secondary forms are described based on the underlying cause, there are many common factors that underlie the development of this segmental injury. In this review, we will describe the currently accepted model for the pathogenesis of classic FSGS and review the data supporting this model. Although the podocyte is considered the major target of injury in FSGS, we will also highlight the contributions of other resident glomerular cells in the development of FSGS.

摘要

局灶节段性肾小球硬化(FSGS)是肾活检时出现的一种组织学损伤模式,可由多种原因和机制引起。虽然根据潜在病因描述了原发性和继发性形式,但这种节段性损伤的发生有许多共同因素。在本综述中,我们将描述目前公认的经典FSGS发病机制模型,并回顾支持该模型的数据。虽然足细胞被认为是FSGS中主要的损伤靶点,但我们也将强调其他肾小球固有细胞在FSGS发生过程中的作用。

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