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  • Title: Immunoglobulin classes and complement in biopsies of Nigerian children with the nephrotic syndrome.
    Author: Houba V, Allison AC, Adeniyi A, Houba JE.
    Journal: Clin Exp Immunol; 1971 May; 8(5):761-74. PubMed ID: 4103296.
    Abstract:
    Pretreatment diagnostic renal biopsies from fifty Nigerian children with the nephrotic syndrome were investigated by immunofluorescence for immunoglobulin classes, complement and specific antigens. Nineteen of these were re-examined after an interval of 10–15 months. Forty-eight first biopsies were positive for bound γ-globulins, usually IgM and IgG but sometimes for one of these alone; IgA was not detected. Thirty-three were positive for bound complement (C3 component). IgM was associated with granular deposits and complement, IgG with both granular and continuous deposits, the latter usually lacking complement. Plasmodium malariae antigen was found in nine of thirty-six cases examined; no P. falciparum or streptolysin-O antigens were observed. Immunoglobulins G and M were found in tubules in seventeen of the fifty patients, in five together with complement. P. malariae antigen was observed in tubules in eleven of thirty-six cases. Repeat biopsies from four patients who had recovered were negative with all reagents. Patients on anti-malarial therapy only, and those responding poorly to steroids or cyclophosphamide, showed no significant change in glomerular fluorescence, but a higher incidence of tubular fluorescence was noted in second biopsies. In patients with a poor response to Imuran treatment the pattern of glomerular fluorescence changed from granular to diffuse and tubular staining was not observed. In some patients increased levels of antiglobulins (rheumatoid factor type) were detected in later sera. The nature of the bound immunoglobulins was confirmed by elution of complexes and immunodiffusion. It is suggested that an antigen–antibody complex with P. malariae antigen can produce renal damage with liberation of autoantigens which have the capacity to initiate self-perpetuating autoimmune disease.
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