McCausland I P, Herdson P B, Gavin J B
Pathology. 1976 Apr;8(2):117-26. doi: 10.3109/00313027609094437.
Human glomerular basement membrane (GBM) emulsified in Freund's complete adjuvant was injected into 16 Holtzman rats. Eleven (69%) of them subsequently developed glomerulonephritis. This disease was characterized by glomerular changes which included focal lobular hypercellularity due to localized hyperplasia of intracapillary (mesangial or endothelial) cells which often obstructed glomerular capillaries. Later, affected lobules showed necrosis of intracapillary cells, and capillary lumina were filled with homogeneous eosinophilic material. An immunoperoxidase technique revealed autologous anti-GBM antibody in all 3 layers of the GBM and in some regions it was present in greater amount in the lamina rara interna and externa than in the lamina densa. Experimental auto-immune glomerulonephritis in the rat is thus characterized morphologically by a focal proliferative glomerulonephritis which proceeds to focal glumerulosclerosis.
将人肾小球基底膜(GBM)乳化于弗氏完全佐剂中,注射到16只霍尔茨曼大鼠体内。其中11只(69%)随后发生了肾小球肾炎。该疾病的特征是肾小球发生变化,包括由于毛细血管内(系膜或内皮)细胞局部增生导致的局灶性小叶细胞增多,这常常阻塞肾小球毛细血管。后来,受累小叶显示毛细血管内细胞坏死,毛细血管腔充满均匀的嗜酸性物质。免疫过氧化物酶技术显示,在GBM的所有三层中均存在自体抗GBM抗体,并且在某些区域,内、外疏松层中的抗体量比致密层中的更多。因此,大鼠实验性自身免疫性肾小球肾炎在形态学上的特征是局灶性增生性肾小球肾炎,进而发展为局灶性肾小球硬化。