Mice of various inbred strains spontaneously and uniformly develop progressive intercapillary glomerulosclerosis, a mild glomerular disease, upon aging. A study of three mouse strains demonstrated early glomerular lesions including mesangial hyperplasia, granular deposits of immunoglobulin and complement along glomerular capillary walls in the kidneys of mice over 4 mo of age. In addition to the renal pathology, other abnormalities previously described in mice of the “autoimmune” NZB strain were demonstrated. Perivascular lymphoid infiltration of various organs, antinuclear autoantibodies, and antiskeletal muscle autoantibodies were frequently observed in older mice. Circulating antierythrocyte autoantibodies were detected in 33% of old C57BL/6 mice; and these autoantibodies were also demonstrated in significant concentration in kidney eluates. The data suggests a specific autologous immune complex mechanism involving antierythrocyte autoantibodies in the pathogenesis of the glomerular lesions.
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