Matsui K
Department of Immunology, Niigata University School of Medicine, Japan.
Virchows Arch B Cell Pathol Incl Mol Pathol. 1988;56(3):141-52.
Rats immunized with an emulsion of Engelbreth-Holm-Swarm (EHS) tumour and Freund's complete adjuvant (FCA) excreted large amounts of urinary protein from the 14th week after the initial immunization. The amount of urinary protein increased progressively and, after 1 year, reached over 1 g/day. Kidneys removed from immunized rats at 10 weeks, 24 weeks and 1 year after the initial immunization were examined by immunofluorescence, light and electron microscopy. By immunofluorescence microscopy, granular deposits of rat immunoglobulins (Igs) were observed along the glomerular capillary walls from the 10th week until the end of the observation period. Glomerular membranous transformation was observed from the 24th week by light microscopy. The glomerular capillary walls were thickened and argyrophilic spikes and vacuolations were detected. At 1 year the severity of these changes was increased. Electron microscopic examination showed only a few electron-dense deposits after 10 weeks, but after 24 weeks numerous electron-dense deposits were detected in all glomeruli, the glomerular basement membrane was thickened and irregular and podocyte foot processes were effaced. At 1 year, dense deposits were located intramembranously and their density decreased from the circumference to the centre. Lesions characteristic of human membranous nephritis were observed in this model, the appearances at 10 weeks, 24 weeks and 1 year corresponding to stages I, II and III, respectively, of the classification of Ehrenreich and Churg (1968). Comparison of the immunohistochemical abnormalities in this model and in Heymann nephritis revealed antigenic cross-reactivity; there appears to be common antigenicity between the immune deposits in the glomeruli in both models, cell surface antigens in the EHS tumour and those located in the cell surface antigens in the brush borders of proximal convoluted tubules. Although the antigens responsible have not yet been clearly identified, in this paper I describe a new model of membranous nephritis, tentatively termed EHS nephropathy.
用恩格尔布雷特 - 霍尔姆 - 斯旺（EHS）肿瘤与弗氏完全佐剂（FCA）的乳剂免疫的大鼠，在初次免疫后第14周开始排出大量尿蛋白。尿蛋白量逐渐增加，1年后超过1克/天。在初次免疫后10周、24周和1年时，对免疫大鼠的肾脏进行免疫荧光、光学和电子显微镜检查。通过免疫荧光显微镜检查，从第10周直到观察期结束，在肾小球毛细血管壁上观察到大鼠免疫球蛋白（Ig）的颗粒状沉积物。光学显微镜下从第24周开始观察到肾小球膜性转化。肾小球毛细血管壁增厚，检测到嗜银性钉突和空泡形成。1年时这些变化的严重程度增加。电子显微镜检查显示，10周后仅发现少量电子致密沉积物，但24周后在所有肾小球中均检测到大量电子致密沉积物，肾小球基底膜增厚且不规则，足细胞足突消失。1年时，致密沉积物位于膜内，其密度从周边向中心降低。在该模型中观察到了人类膜性肾病的特征性病变，10周、24周和1年时的表现分别对应于埃伦赖希和丘格（1968年）分类中的I期、II期和III期。该模型与海曼肾炎免疫组织化学异常的比较显示存在抗原交叉反应；两种模型肾小球中的免疫沉积物、EHS肿瘤中的细胞表面抗原与近端曲管刷状缘细胞表面抗原之间似乎存在共同抗原性。尽管尚未明确鉴定出相关抗原，但在本文中我描述了一种新的膜性肾病模型，暂称为EHS肾病。
