Interstitial immune complex nephritis in patients with systemic lupus erythematosus (SLE). Renal tissues from 45 patients with SLE nephritis, 34 patients with idiopathic membranous nephropathy (IMN) and 77 patients with minimal glomerular disease (MGD) were studied by light, immunofluorescence and electron microscopy. Interstitial nephritis characterized by focal or diffuse infiltration of inflammatory cells, tubular damage and interstitial fibrosis was observed in 66% of SLE patients. Fluorescein-conjugated antibodies to immunoglobulins or complement or both were bound to peritubular capillaries, interstitium and tubular basement membranes (TBM) in 53% of patients with a granular pattern corresponding to opaque deposits seen by light or electron microscopy or both. Antibodies reactive with thymidine or cytosine or both were bound to interstitial structures in 19% of patients tested and showed the same granular distribution. Interstitial cellular infiltration was rare and deposits of immunoglobulins and complement were rare or absent in IMN and MGD, whereas deposits of DNA products were never observed. The findings are consistent with the interpretation that in patients with SLE nephritis immune deposits, presumably containing DNA-anti-DNA complexes, localize in peritublular capillaries, TBM and interstitum, thereby producing an inflammatory reaction which contributes to development and evolution of renal diseases.

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.