ヒト慢性糸球体腎炎例における糸球体結合性の抗腎基底膜活性IgGの存在について

抄録

The main purpose of this article is to investigate the immunological back ground in the pathogenesis of human chronic glomerulonephritis. At the first step, the existence of cross-antigenisities among the mammalias especially between human and rat renal basement membranes was proven through the following experimental evidence that in vivo administrated anti human renal basement membrane rabbit serum to rats was fluorescent microscopically found to be immediately fixed linearly along the rat renal glomerular basement membranes, forming regional focal immune complexes, and simultaneously focal glomerulonephritis was produced. The antigenic determinants in the glomerular capillary basement membrane at this occasion was thought to be located in trypsin or collagenase digestion resistant macro-molecular ingredients of the basement membrane. In the human chronic glomerulonephritic kidneys obtained at autopsies, fluorescent microscopical examinations revealed that IgG fraction was rarely but serum complement component was frequently bound linearly along the glomerular capillary basement membranes. On the contrary, the eluted materials from the chronic glomerulonephritic kidneys under acidic citric buffer contained IgG fraction in high percentages. Furthermore, such eluted IgG from the glomerulonephritic kidneys showed capacity to combine focally with rat glomerular capillary basement membranes, to form immune complexes and develop transient proliferative focal glomerulonephritis after in vivo administration to rats. The sera from the chronic glomerulonephritic cases or the eluted materials from several control kidneys which although contained some IgG fractions, revealed no such in vivo reactivities to rat renal glomeruli. From the above findings, it was thought that eluted IgG from the human chronic glomerulonephritic kidneys might have had in vivo glomerular basement membrane bound activity even in their own kidneys, although could not be demonstrated by immuno-fluorescent examination. Successively formed regional immune complexes might have given incessant pathogenic effects upon glomeruli, which led to progressive chronic glomerulonephritis. The autoimmune nature in pathogenesis of this disease could be well compared to that of the experimental nephrotoxic serum nephritis and furthermore, this pathogenic process was frankly represented clinically on the occurrence of proliferative glomerulonephritis in the transplanted kidneys to the chronic glomerulonephritic patients.