抄録
As a model of human membranous nephropathy, passive Heymann nephritis (PHN) was established in female Sprague-Dawley rats by intraperitoneal injection of rabbit antirat FxlA serum. Morphological studies with lightmicroscope (LM), immunofluorescent microscope (IF) and electron. microscope (EM) were done 1 hour through 6 months after anti-Fx1A serum injection. Also the presence of a FxlA like antigen in rat glomeruli was studied using indirect immunofluorescence and solid phase radioimmunobinding test. Two phases were noticed. First (heterologous) phase was characterized by mild proteinuria on day 5 through 10 (54±9mg/day, mean+S.D.) and diffuse granular staining of rabbit gamma-globulins and rat C3 along glomerular capillary walls. Second (autologous) phase was accompanied with more prominent proteinuria (152±28mg/day), the deposition of rat IgG in addition to rabbit gamma-globulins and the disappeappearance of rat C3. Observation on EM disclosed the sequential changes of the subepithelial deposits whichh were similar to the staging of human membranous nephropathy. Initially amorphous deposits, then well demarcated ones associated with thickening of GBM and finally lucentt ones were observed. By indirect IF on the frozen sections, normal rat glomeruli did not show any specificc binding with anti-FxIA antibody even after removal of surface glycoproteins by neuroaminidase. However, isolated rat glomeruli and their sonicated fractions binded the antibody significantly by IF and solid phase radioimmunobinding test. Thus, it is concluded that the initial mechanism of PHN is in situ immune complex formation between anti-FxIA antibody and a glomerular FxIA like antigen, while superimposed deposition of autologous antibodies against rabbit gamma-globulins seems to play an additional important role in persistance of PHN.
