Sinclair R A, Antonovych T T, Mostofi F K
Hum Pathol. 1976 Sep;7(5):565-88. doi: 10.1016/s0046-8177(76)80103-7.
This presentation reports the light and electron microscopic findings relating to the vascular and glomerular changes in the kidney in a series of 25 patients having malignant hypertension, the hemolytic-uremic syndrome, scleroderma, or toxemia of pregnancy. The pathologic changes were generally similar in each of the diseases studied, the changes being related more to the severity and duration of injury than to the specific disease. Vascular narrowing was due mainly to intimal thickening, and by light microscopy the lesions were categorized as onionskin, mucinous, or fibrous with or without associated elastosis. Intimal erythrocyte extravasation, fibrinoid necrosis, and luminal thrombosis were also seen. Electron microscopy provided additional morphologic information: Myointimal cells were found to be the cellular component in each type of intimal thickening; it was possible to distinguish collagen from large intimal accumulations of basement membrane material; mucinous intimal material was characterized ultrastructurally; and fibrinoid necrosis was identified as a lesion inconstantly associated with cellular necrosis and consisting mainly of fibrinoid material and small deposits of fibrin. It seems likely that there is a common pathogenesis for intimal thickening in a variety of diseases and that this involves endothelial cell damage and increased permeability, leakage of serum and erythrocytes into the intima, and a healing reaction of the vessel wall was developing from migration of smooth muscle cells into the intima with subsequent myointimal cell proliferation and fibrogenesis. A common glomerular change in all diseases studied was a striking accumulation of electron lucent material between the endothelium and the lamina densa of the basement membrane. This lesion was interpreted as a manifestation of acute ischemia.
本报告阐述了对25例患有恶性高血压、溶血尿毒综合征、硬皮病或妊娠中毒症患者肾脏血管和肾小球变化的光镜及电镜观察结果。在所研究的每种疾病中，病理变化总体相似，这些变化更多地与损伤的严重程度和持续时间有关，而非特定疾病。血管狭窄主要归因于内膜增厚，光镜下病变可分为洋葱皮样、黏液样或纤维样，有无弹性组织变性。还可见内膜红细胞外渗、纤维蛋白样坏死和管腔内血栓形成。电镜提供了更多形态学信息：肌内膜细胞是每种内膜增厚类型的细胞成分；能够区分胶原与大量内膜基底膜物质积聚；黏液样内膜物质具有超微结构特征；纤维蛋白样坏死被确认为一种与细胞坏死不恒定相关的病变，主要由纤维蛋白样物质和少量纤维蛋白沉积组成。多种疾病内膜增厚似乎存在共同的发病机制，这涉及内皮细胞损伤和通透性增加、血清和红细胞漏入内膜，以及血管壁的愈合反应，即平滑肌细胞迁移至内膜，随后肌内膜细胞增殖和成纤维。所有研究疾病中常见的肾小球变化是基底膜内皮和致密层之间显著积聚电子透亮物质。此病变被解释为急性缺血的表现。
