1973 Volume 15 Issue 8 Pages 763-772_2
Attempts were made to demonstrate circulating autoantibodies against the kidney of 42 patients in terminal stage of glomerulonephritis controlled by maintenance dialysis. To detect antibodies, cryostat sections of normal kidney of blood group 0 individual were incubated with patient sera, and the bound immunoglobulins were stained with fluorescent antiglobulin reagents. As the results, 3 cases with autoantibodies against tubular cells and 1 case with antinuclear antibody were found. Anti-glomerular basement membrane antibodies (anti-GBM) were negative in all cases including 6 nephrectomied-anephric patients. However, some sera reacted with the glomerular and in-tertubular capillaries in the manner as though indicating the presence of anti-GBM. This false positive reaction occurred only in the combination of special blood groups : the serum (0 type) and the kidney (A type). These data warrant the greatest possible care to differentiate the true autoantibodies from allo- and heterophilic antibodies. The selection of detecting antigens as well as the use of a panel of antigens obtained from different sources are highly recommended. All the anti-tubular cytoplasmic antibodies in the 3 sera were complement fixing IgG, and directed to the same antigen. This antigen was distributed not only in tubuli, but in gastric and intestinal mucosa of all the mammalian species tested, including humans, rats, rabbits, mice and guinea pigs. Differential centrifugation study revealed the exclusive localization of the antigen in microsome fraction. This antibody (tubular microsomal antibody) cannot be discriminated from the mitochondrial antibody (Doniack 1966) in the routine screening by immunofluorescence utilizing kidney sections as detecting antigen because of the similarity of specific staining with both antisera in the cytoplasma of tubular epithelia. Although the tubular microsomal antibody reported here has not been described, it may well have been overlooked for this reason. It would be necessary to identify mitochondrial antibodies not only by the traditional immunofluorescent method using kidney sections, but also by the more detailed study of the corresponding antigen by means of the above mentioned methods. The possibility of the tubular microsomal antibody in producing antigen-antibody complex and thus mediating glomerulonephritis is currently under our investigations through the elution study of this anti-body from the diseased kidney.
