大鼠加速型抗肾小球基底膜（GBM）肾炎的研制

将正常兔ＩｇＧ与完全弗氏佐剂颈免疫大鼠，８天后注射亚致肾炎剂量的兔抗大鼠肾小球基底膜（ＧＢＭ）血清，结果大鼠尿蛋白量在注射该血清后第１天即明显升高，第３天达高峰；在第２１天时，血清肌酐显著升高。肾脏组织学检查：免疫荧光见第１天即有大鼠ＩｇＧ、Ｃ３和兔ＩｇＧ沿ＧＢＭ呈典型线状沉积；光镜见第１天肾小球内细胞数目明显增加，内皮细胞肿胀，肾小球内见中性粒细胞浸润，第７、１４．２１天时肾小球毛细血管丛系膜区增宽，系膜细胞增生，间质可见炎症细胞浸润，ＰＡＳＭ染色可见ＧＢＭ增厚，电镜见ＧＢＭ内有电子致密物线状沉积，上皮足突融合内皮窗孔消失，微血栓形成阻塞管腔，间质有细胞浸润和纤维化。

The Development of the Rat Model of AcceleratedAnti-GBM Glomerulonephritis

he subnephritogenic dose of nephrotoxic serum was injected into therat that was preimmunized with normal rabbit IgG in complete Freund's adju-vant eight days before.The results showed that the proteinuria of the ratwas obvious on the first day, and the peak proteinuria occurred on the thirdday.On the 21th day, serum creatinine ( Scr ) was significantly enhanced.The renal histological changes:By immunofluorescence, the main findings onthe first day was thedeposition of rat IgG, C3 and rabbit IgG along CBM.By light microscopy, the number of the cells in the glomerulus on the firstday was significantly increased, with endothelial cells swollen and neutroph-ils infiltrated.On the 7th, 14th, 21th days, the mesangium of the glomerulcapillaries ware widened; mesangial cells proliferated, and there were infi-ltration of inflammatory cells in the interstium.CBM was thicker by PASM stain.By electron microscopy,there were electronic dense deposits in GBM.Thefoot processes of epithelial cell disappeared. The capillary lumens wereblocked by thrombi.In the interstitium: there were inflammatory cells andfibrosis .