[Pathogenesis of acute glomerulonephritis].
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Biomedical subjects
Publications and source records attributed to G Treser.
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Fluorescein-labeled immunoglobulin G (IgG) fractions of serum from patients with acute poststreptococcal glomerulonephritis stained parts of the glomerular basement membrane and mesangium of kidney tissue obtained from the same patients during the early phase of the disease. Renal tissue obtained from normal individuals and from patients with other kidney diseases failed to stain with these IgG fractions. Preabsorption of the serum fractions with various freezethawed bacteria demonstrated that only certain group A streptococci abolished the staining capacity. Fractionation of the streptococci into cellular constituents indicated that it was predominantly the plasma membrane fraction which blocked the immune staining. Spectrofluorometry using alkali-solubilized renal tissue confirmed these observations in a quantitative manner. By sucrose density-gradient ultracentrifugation of the plasma membrane two possible antigens were isolated. One was soluble in phosphate-buffered saline and the other was insoluble. The soluble component was a lipoprotein with a molecular weight of approximately 120,000.
Fluorescein-labeled immunoglobulin G fractions from serums of patients with acute glomerulonephritis and from many normal serums stained the glomerular basement membrane and mesangium of renal tissue from patients with early acute glomerulonephritis; these serums did not stain the corresponding tissues from patients with any other kidney disease. Previous absorption of the serum fraction with frozen and thawed nephritogenic beta hemolytic streptococci abolished all staining. Other bacteria studied did not abolish the staining. Only the plasma membrane of the streptococcus absorbed the immunoglobulin G fraction; such absorption eliminated staining. Fluorescein-labeled antiserums against streptococcal plasma membrane had staining properties similar to patients' serums.
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To investigate the role of circulating immune complexes (CIC) in the pathogenesis of acute poststreptococcal glomerulonephritis (AGN), sera were obtained serially from 13 patients with biopsy-proven AGN, 16 patients with group A streptococcal infection, and 20 age- and sex-matched controls. Samples were analysed for Clq-binding activity (Clq-BA), levels of IgG, IgA, IgM, C3 and C4, and antibody titres to streptococcal enzymes. Significant elevation of Clq-BA was observed in 11 patients (84.5%) with AGN and 7 patients (44%) with streptococcal infection alone. The data suggest that CIC do not necessarily cause glomerular damage, but rather represent a systemic inflammatory response in patients with group A streptococcal infection.
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