Cavallo T, Goldman M, Graves K, Lambert P H
Kidney Int. 1983 Nov;24(5):632-7. doi: 10.1038/ki.1983.204.
We investigated the pathogenesis of increased glomerular permeability in Balb/c mice after 5 weeks of administration of a polyclonal B cell activator (bacterial lipopolysaccharide). The glomerular transfer of anionic ferritin across the capillary walls and the urinary excretion of serum albumin served as probes of glomerular permeability; anionic groups of the glomerular basement membrane were assessed by the binding of cationized ferritin, and glomeruli were studied by light, immunofluorescence, and electron microscopy. The mice developed circulating immune complexes, proteinuria, and a proliferative glomerulonephritis, with mesangial and capillary loop deposits of immunoreactants. Increased transfer of anionic ferritin molecules occurred across capillary walls with and without demonstrable electron-dense deposits; detachments of visceral epithelium were not seen, and epithelial transport of anionic ferritin was negligible. Loss of anionic groups was extensive in glomerular capillary loops with and without associated electron-dense deposits. The findings indicate that an increase in glomerular permeability may precede the deposition of immunoreactants in the capillary wall; that filtration of macromolecules can occur across capillary walls with or without demonstrable immune deposits; and that loss of anionic groups of the glomerular basement membrane and enhanced filtration of macromolecules can occur in the absence of focal detachments of the visceral epithelium.
我们研究了在给予多克隆B细胞激活剂（细菌脂多糖）5周后，Balb/c小鼠肾小球通透性增加的发病机制。阴离子铁蛋白跨毛细血管壁的肾小球转运以及血清白蛋白的尿排泄作为肾小球通透性的指标；通过阳离子化铁蛋白的结合来评估肾小球基底膜的阴离子基团，并通过光学显微镜、免疫荧光显微镜和电子显微镜对肾小球进行研究。小鼠出现循环免疫复合物、蛋白尿和增殖性肾小球肾炎，免疫反应物沉积于系膜和毛细血管袢。无论有无可证实的电子致密沉积物，阴离子铁蛋白分子跨毛细血管壁的转运均增加；未观察到脏层上皮细胞脱离，阴离子铁蛋白的上皮转运可忽略不计。无论有无相关电子致密沉积物，肾小球毛细血管袢中阴离子基团的丢失均广泛存在。这些发现表明，肾小球通透性增加可能先于免疫反应物在毛细血管壁的沉积；大分子物质可通过有或无可证实免疫沉积物的毛细血管壁进行滤过；并且在没有脏层上皮细胞局灶性脱离的情况下，肾小球基底膜阴离子基团的丢失和大分子物质滤过增加也可发生。
