大鼠加速型抗肾小球基膜肾炎的研制

The development of the rat model of accel-erated anti-GBM glomerulonephritis

将正常兔ＩｇＧ与完全弗氏佐刑预免疫大鼠８天后注射亚致肾炎剂量的兔抗大鼠肾小球基膜（ＧＢＭ）血清，结果大鼠尿蛋白量在注射该血清后第一天即明显升高，第三天达高峰，在第２１天时，血清肌酐显著升高。肾脏组织学检查：免疫荧光见第一天即有大鼠ＩｇＧ，Ｃ３和兔ＩｇＧ沿ＧＢＭ呈典型线状沉用，光镜见第一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，第七、第１４、第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染色可见到ＧＢＭ增厚，电镜见ＧＢＭ内有电子致密物线状沉积，上皮足突融合，内在窗孔消失，微血栓形成阻塞管腔、间质有细胞浸润和纤维化。

he subnephritogenic dose of nephro-toxic serum was injected into the rat preim-muned with normal rabbit IgG in completeFreundis adjuvant & days before. The re-sults showed that the proteinuria of the ratwas obvious at the first day,and peaked atthe 3rd day. At the Zlst day, serum creati-nine (Scr) significantly enhanced. The renalhistological changes induded: at the first daythere were the depositions of rat IgG ,C3 andrabbit IgG along GBM by immunofluo-rescence by light microscope,the nu'nber ofthe cells in the glomerulus at the first daysignificantly increased with endothelial cellsswollen and neutrophils infiltration. At the7th 14th and 21st days,the mesangium ofthe glomerular capillaries widen; mesangialcells proliferated,and there were infiltrationof inflamznatorry cells in the interstium.GBM was thicker by PASM stain, By elec-tron microscope,there were electronic densedeposits in GBM. The foot processes of ep-ithelial cell disappeared. The capillary lu-rnens were blocked by thrombi. In the in-terstitium, there were inflammatory cellsand fibrosis.