Trimarchi Hernán
Hernán Trimarchi, Servicio de Nefrología, Hospital Británico de Buenos Aires, Buenos Aires 1280, Argentina.
World J Nephrol. 2013 Nov 6;2(4):103-10. doi: 10.5527/wjn.v2.i4.103.
Primary focal and segmental glomerulosclerosis (FSGS) may be due to genetic or acquired etiologies and is a common cause of nephrotic syndrome with high morbidity that often leads to end-stage renal failure. The different available therapeutic approaches are unsuccessful, in part due to partially deciphered heterogeneous and complex pathophysiological mechanisms. Moreover, the term FSGS, even in its primary form, comprises a histological description shared by a number of different causes with completely different molecular pathways of disease. This review focuses on the latest developments regarding the pathophysiology of primary acquired FSGS caused by soluble factor urokinase type plasminogen activator receptor, a circulating permeability factor involved in proteinuria and edema formation, and describes recent advances with potential success in therapy.
原发性局灶节段性肾小球硬化(FSGS)可能由遗传或后天病因引起,是肾病综合征的常见病因,发病率高,常导致终末期肾衰竭。现有的不同治疗方法均未成功,部分原因是其异质性和复杂的病理生理机制尚未完全阐明。此外,FSGS这一术语,即使是其原发性形式,也包含了多种不同病因共有的组织学描述,而这些病因具有完全不同的疾病分子途径。本综述聚焦于由可溶性因子尿激酶型纤溶酶原激活物受体引起的原发性获得性FSGS的病理生理学最新进展,该受体是一种参与蛋白尿和水肿形成的循环通透性因子,并描述了在治疗方面可能取得成功的最新进展。