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Twenty-seven patients with diffuse "crescentic" glomerulonephritis (CSGN) were identified in 1,174 renal biopsies from nephritic patients. Patients were assigned to three groups on the basis of the immunofluorescent study of renal biopsy specimens and serologic findings. Group I included eight patients with antibodies to glomerular (anti-GBM) and tubular (anti-TBM) basement membranes; group II had eight patients with only anti-GBM antibodies; and group III had eleven patients with CSGN unassociated with antibodies to either GBM or TBM. Patients with anti-GBM/anti-TBM antibodies (group I) had severe tubulointerstitial (TI) nephritis, as characterized by the infiltration of polymorphonuclear leukocytes and macrophages along the TBM and peritubular vessels. In some patients, focal proliferation of epithelial cells of proximal convoluted tubules (PCT), gaps or extensive destruction of TBM, lesions in the walls of small peritubular vessels, and interstitial giant cells were also observed. Patients with anti-GBM antibodies (group II) had mild to moderate interstitial cellular infiltration and mild tubular changes. Five patients with CSGN not associated with antibodies to renal basement membranes (group III) had mild to moderate interstitial cellular infiltration and tubular changes. A sixth patient, with Wegener's disease had severe granulomatous TI lesions. The results of this study show that TI nephritis is most frequent and severe with anti-TBM antibodies are demonstrable and suggest that anti-TBM antibodies contribute to the development of TI lesions.

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 graft.

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