Arnold S B, Valone J A, Askenase P W, Kashgarian M, Freedman L R
Lab Invest. 1975 Jun;32(6):681-9.
Intravenous administration of live microorganisms to rabitts with cardiac catheters produces an experimental model of infective endocarditis. Despite the development of infected valvular vegetations, positive blood cultures, splenomegaly, and focal embolic renallesions, glomerulonephritis has not been found in these animals. In the present study, acute diffuse proliferative glomerulonephritis, featuring endothelial and mesangial proliferation, capillary occlusion, and leukocytic infiltration was produced in rabbits immunized withthe infecting agent prior to the establishment of left sided alpha-streptococcal endocarditis. Controls receiving immunization alone, immunization and sterileendocarditis, or infective endocarditis alone did not develop diffuse glomerulonephritis. Electron microscopic findings of occasional subendothelial electron-dense deposits and immunofluorescence deposition of IgG and C3 in a peripheral granular capillary pattern were consistent with an immune complex type nephritis. Decreased serum complement levels were demonstrated in those animals developing diffuse glomerulonephritis, and some animals developed circulating rheumatoid factor. In view of the morphologic findings and the necessity of preimmunization for development of glomerular changes, it is concluded that immune mechanisms play a role in the diffuse glomerulonephritis associated with this model of infective endocarditis.
通过心脏导管向兔子静脉注射活微生物可产生感染性心内膜炎的实验模型。尽管出现了感染性瓣膜赘生物、血培养阳性、脾肿大和局灶性栓塞性肾损害，但在这些动物中未发现肾小球肾炎。在本研究中，在左侧α-链球菌性心内膜炎形成之前，用感染因子免疫的兔子出现了以内皮细胞和系膜细胞增生、毛细血管闭塞和白细胞浸润为特征的急性弥漫性增生性肾小球肾炎。仅接受免疫、免疫和无菌性心内膜炎或仅感染性心内膜炎的对照组未发生弥漫性肾小球肾炎。偶尔出现的内皮下电子致密沉积物的电子显微镜检查结果以及IgG和C3以周边颗粒状毛细血管模式的免疫荧光沉积与免疫复合物型肾炎一致。在发生弥漫性肾小球肾炎的动物中，血清补体水平降低，一些动物出现循环类风湿因子。鉴于形态学发现以及肾小球变化发生需要预先免疫，得出结论：免疫机制在与这种感染性心内膜炎模型相关的弥漫性肾小球肾炎中起作用。
