Necrotizing glomerulitis of systemic lupus erythematosus.
The authors report four cases of systemic lupus erythematosus (SLE) with severe, active glomerulonephritis. Associated with histologic evidence of glomerular inflammation were focal, predominantly mesangial immune reactants. This finding contrasts with reports that massive subendothelial electron-dense deposits are the ultrastructural feature that correlates best with the severity of glomerular inflammation. The patients studied had significantly fewer subendothelial electron-dense deposits than did other patients with SLE with comparable glomerular lesions (8 +/- 3 per cent versus 42 +/- 14 per cent of glomerular capillaries involved, respectively; P less than 0.05). In addition, serologic evidence of disease activity, assessed by measurement of serum levels of C3, C4, circulating immune complexes (cryoglobulins), and serum antinative DNA activity, was either normal or only mildly abnormal. The lack of correlation between the severity of glomerular lesions on the one hand and the paucity of glomerular immune reactants and mild serologic abnormalities on the other may be interpreted as questionable evidence that these cases of glomerulonephritis were mediated by immune complexes. In the light of recent clinical and experimental studies that support a possible role for cell-mediated immunity in the pathogenesis of glomerulonephritis, the authors propose that a role for cell-mediated hypersensitivity be considered.
D005921:Glomerulonephritis / Q000209:etiology* / Q000276:immunology; D006801:Humans; D007136:Immunoglobulins / Q000032:analysis; D007678:Kidney Glomerulus / Q000648:ultrastructure; D008180:Lupus Erythematosus, Systemic / Q000150:complications*; D009336:Necrosis; D000511:alpha-Macroglobulins / Q000032:analysis
D007136:Immunoglobulins; D000511:alpha-Macroglobulins