• 1 January 1981
    • journal article
    • research article
    • Vol. 44  (1) , 1-5
Abstract
The pathogenesis of Heymann nephritis (HN), a morphologic and immunohistologic model for the human membranous glomerulonephropathy, is controversial. To determine the presence of the offending antigen in glomeruli, the specific disease-producing brush border antibody (BBAb) of homologous origin was infused into isolated perfused rat kidney. The antibody was obtained from the acid kidney eluates from rats with severe HN and purified using ion exchange and gel filtration chromatography. Its molecular size and IgG nature were ascertained by gel filtration, sucrose density gradient ultracentrifugation, and immunoelectrophoresis, and its specificity by indirect immunofluorescence. Isolated perfused kidneys were perfused with 0.5-10 mg of BBAb; 3 control groups were perfused with buffer only, normal rat IgG, and BBAb absorbed with a renal cortical fraction FX1A, respectively. The ischemia time ranged from 24-34 min. BBAb localization was noted in glomerular capillaries and mesangium and in the walls of blood vessels of many sizes. Normal rat IgG and absorbed BBAb did not show any localization. Evidently the putative HN antibody when injected into a perfused, bloodless, ischemic kidney combines specifically with an antigen which is present in the glomerular capillaries and other blood vessels. Although this represents in situ immune complex formation, which may be suspected of occurring in active HN, the conditions of the isolated perfused kidney under which this occurs are clearly unphysiologic. Whether it occurs in the physiologic in vivo state will require further studies.