Shibata S, Sakaguchi H, Nagasawa T
Contrib Nephrol. 1975;4:22-35.
Proliferative glomerulonephritis was induced in rats by a single injection in the hind footpads of the urinary glycoprotein or more purified urinary glycopeptide with Freund's incomplete adjuvant. Although the urinary (water-soluble and non-dialyzable) glycoprotein and glycopeptide were prepared from heterologous urines (human urines), the immunofluorescent pattern of the kidneys was not 'granular' but 'mesangial', as in rats given a single injection of homologous or heterologous renal glycoprotein with nephritogenicity. The pathogenesis of proliferative glomerulonephritis in the present experiments may be explained by the same mechanism as that of rats given a single injection of renal glycoprotein, i.e. by any mechanism other than antigen (heterologous protein)-antibody immune complex and anti-GBM antibody mechanisms.
通过在大鼠后足垫单次注射尿糖蛋白或更纯化的尿糖肽与弗氏不完全佐剂，诱导大鼠发生增殖性肾小球肾炎。尽管尿（水溶性且不可透析的）糖蛋白和糖肽是从异源尿液（人尿）中制备的，但肾脏的免疫荧光模式并非“颗粒状”而是“系膜性”，就如同给大鼠单次注射具有致肾炎性的同源或异源肾糖蛋白时一样。本实验中增殖性肾小球肾炎的发病机制可能与给大鼠单次注射肾糖蛋白的机制相同，即通过除抗原（异源蛋白）-抗体免疫复合物和抗肾小球基底膜抗体机制之外的任何机制来解释。
