局灶节段性肾小球硬化形成机制及其在IgA肾病中的作用  

Pathogenic Mechanisms of the Focal Segmental Glomerulosclerosis and Its Role in the Progression of IgA Nephropathy

作　　者：陈振杰[1] 李超[1] 李航[1] 李学旺[1] CHEN Zhenjie;LI Chao;LI Hang;LI Xuewang(Department of Nephrology,PUMC Hospital,CAMS and PUMC,Beijing 100730,China)

机构地区：[1]中国医学科学院,北京协和医学院,北京协和医院肾内科,北京100730

出　　处：《中国医学科学院学报》2018年第4期549-555,共7页Acta Academiae Medicinae Sinicae

摘　　要：局灶节段肾小球硬化(FSGS)是肾脏病变中常见的一个病理改变,可因原发性因素或多种继发性因素导致,其形成机制一直是肾脏病研究领域的一个热点。FSGS样病理改变在IgA肾病中发挥重要的预后作用,既往对其形成机制有假说考虑或与血流动力学及足细胞损伤等有关,但是有待研究证实,本文主要综述FSGS发病机制及其在IgA肾病中的作用,以期为IgA肾病的治疗提供有益的思路。Focal segmental glomerulosclerosis(FSGS),a common pathological change in kidney diseases,may be caused by primary factors or multiple secondary factors.Its pathogenic mechanism remains a hot topic in kidney disease research.FSGS-like pathologic changes are highly in IgA nephropathy.It has been speculated that FSGS in IgA nephropathy might be caused by hemodynamics changes,and podocyte injury,which,however,have not been well documented.Our current review focuses on the pathogenesis of secondary FSGS and its role in the progression of IgA nephropathy,with an attempt to provide more insights in the treatment of IgA nephropathy.

关 键 词：继发性局灶节段肾小球硬化 IGA肾病 病理机制 

分 类 号：R44[医药卫生—诊断学]