In two patients with chronic glomerulonephritis who received renal allografts, transplant failure was associated with binding of transplantation antibodies to the graft and with glomerular and vascular changes frequently seen in chronic rejection. Lesions of renal tubules were characterized by basement membrane thickening, splitting or disruption, with adjacent extensive mononuclear cell infiltrates. Direct immunofluorescence showed linear staining pattern for IgG, IgA and C3 along the tubular basement membranes of the two allografts and linear staining for IgG in the tubular basement membranes of the own kidneys of one patient who had not been nephrectomized prior to renal transplantation. Indirect immunofluorescence and passive transfer studies demonstrated that theimmunoglobulins eluted from the grafts reacted with the tubular basement membranes of all human and monkey kidneys tested. Since antibodies with similar reactivity would also be eluted from the recipient’s own kidneys, they can be classified as autoantibodies. The presented data, however, do not indicate whether the autoimmune response was induced by the graft or whether the lesion just recurred in the graf
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