Kondo Y, Akikusa B
Acta Pathol Jpn. 1982 Mar;32(2):231-42.
Chronic focal glomerulonephritis was induced in the rat by using goat nephrotoxic IgG. In the later stage (6 to 15 months) a number of glomeruli were found to be attached to Bowman's capsule with variable segmental sclerosis and/or hyalinosis. The morphogenesis of the changes was studied by electron microscopy. It was found that partial cytoplasmic necrosis of podocytes was an initiating event of the capsular adhesion. When this occurred in the peripheral tufts, the denuded portion of the glomerular basement membrane (GBM) became attached to the parietal epithelium, resulting in progressive thickening of the mesangium and GBM, deposition of hyaline or proteinaceous material, and desquamation of the endothelial sheet, the features being compatible with segmental glomerular sclerosis and/or hyalinosis. It seemed that these changes, in turn, accelerated podocyte desquamation and extension of the capsular adhesion, producing a progressive cycle that terminated in global glomerular hyalinosis. Such a sequence of events most often occurred in rats with massive proteinuria, suggesting that persistent, severe proteinuria caused the podocyte lesion which led to the development of segmental glomerular sclerosis and/or hyalinosis.
采用山羊肾毒性IgG诱导大鼠发生慢性局灶性肾小球肾炎。在后期（6至15个月），发现许多肾小球与鲍曼囊附着，伴有不同程度的节段性硬化和/或玻璃样变性。通过电子显微镜研究了这些变化的形态发生过程。发现足细胞的部分细胞质坏死是囊粘连的起始事件。当这种情况发生在周边肾小球时，肾小球基底膜（GBM）的裸露部分与壁层上皮附着，导致系膜和GBM逐渐增厚，透明或蛋白质样物质沉积，以及内皮细胞层脱落，这些特征与节段性肾小球硬化和/或玻璃样变性相符。似乎这些变化反过来又加速了足细胞脱落和囊粘连的扩展，形成一个渐进的循环，最终导致整个肾小球玻璃样变性。这样一系列事件最常发生在有大量蛋白尿的大鼠中，提示持续性严重蛋白尿导致足细胞损伤，进而导致节段性肾小球硬化和/或玻璃样变性的发生。
