Shigematsu H, Dikman S H, Churg J, Grishman E, Duffy J L
Am J Pathol. 1976 Nov;85(2):349-62.
Electron microscopic analysis of the mesangial injury in the hemolytic-uremic syndrome was performed in 10 patients. Proteinaceous material similar to that found in the subendothelial region was also seen focally in the mesangium altering the matrix and imparting a reticular appearance. This degenerative process was associated with reparative changes in the glomerular tuft. Many of the mesangial cells were hypertrophied and demonstrated phagocytic activity and peripheral extension of their cytoplasmic processes. Mitotic figures in endothelial as well as mesangial cells were regarded as evidence of a reparative process. Severe mesangial insudation of material containing fibrinogen derivatives resulted in segmental tuft necrosis with almost complete replacement and destruction of the mesangial matrix. On some occasions, a break of the glomerular basement membrane was accompanied by the escape of intraluminal contents into the urinary space, leading to crescentic epithelial cell proliferation.
对10例溶血尿毒综合征患者的系膜损伤进行了电子显微镜分析。在系膜中也局灶性地观察到类似于在内皮下区域发现的蛋白质物质，其改变了基质并呈现出网状外观。这种退行性过程与肾小球毛细血管丛的修复性变化相关。许多系膜细胞肥大，表现出吞噬活性和细胞质突起的外周延伸。内皮细胞和系膜细胞中的有丝分裂象被视为修复过程的证据。含有纤维蛋白原衍生物的物质严重系膜内渗导致节段性毛细血管丛坏死，系膜基质几乎完全被替代和破坏。在某些情况下，肾小球基底膜破裂伴有管腔内内容物漏入尿腔，导致新月体上皮细胞增殖。
