IMMUNO-HISTOPATHOLOGY OF GLOMERULAR ANTIGENS .2. GLOMERULAR BASEMENT-MEMBRANE, ACTOMYOSIN, AND FIBROBLAST SURFACE-ANTIGENS IN NORMAL, DISEASED, AND TRANSPLANTED HUMAN KIDNEYS

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  • 1 January 1978
    • journal article
    • research article
    • Vol. 90  (1) , 71-88
Abstract
Immunofluorescent studies demonstrated that actomyosin (AMY) is present in the mesangium in a restrictive pattern; fibroblast surface antigen (FSA) has a more extensive mesangial distribution. Antibody to glomerular basement membrane (GBM) is localized to the GBM. Tissue samples [196], including 17 from normal subjects, 94 from patients with primary renal diseases and 85 from transplanted kidneys, were examined for changes in distribution of AMY, FSA and GBM antigens. The distribution of AMY and FSA in the mesangium is markedly increased in width in patients with diabetic nephropathy and the GBM is thickened. AMY and FSA are mildly increased in patients with glomerulonephritis and GBM is normal. Patients with membranoproliferative glomerulonephritis (MPGN) show a loss of all glomerular antigens. Increased mesangial AMY was found in 12 of 37 transplanted kidneys in diabetic patients vs. 4 of 33 nondiabetics 0-4 yr after transplantation (P < 0.025). This difference is more notable at 2-4 yr, with 5 of 9 diabetics showing increased AMY vs. 0 of 6 nondiabetic patients (P < 0.0005). In MPGN, 5 of 8 tissues showed decreased mesangial AMY vs. 3 of 36 diabetic patients (P < 0.0005) and 1 of 32 patients with other glomerulopathies (P < 0.0005). GBM thickening is not associated with specific pretransplant diseases. In transplanted kidneys, the pattern of FSA is dissociated from that of AMY: over half of all patients have increased FSA, even when AMY is normal. Whether this unique finding in transplanted kidneys reflects an increase in the synthesis of FSA by mesangial cells or the failure to clear this (circulating) antigen from the mesangial matrix is unknown.