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Related Experiment Videos

Alternative C3 pathway activiation in pneumococcal glomerulonephritis.

L R Hyman, E H Jenis, G S Hill

    The American Journal of Medicine
    |June 1, 1975
    PubMed
    Summary

    Pneumococcal infection can cause glomerulonephritis. This study suggests pneumococcal polysaccharides activate the alternate complement pathway, leading to kidney inflammation and a limited disease course.

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    COMPLEMENT FIXATION IN DISEASED TISSUES : I. FIXATION OF GUINEA PIG COMPLEMENT IN SECTIONS OF KIDNEY FROM HUMANS WITH MEMBRANOUS GLOMERULONEPHRITIS AND RATS INJECTED WITH ANTI-RAT KIDNEY SERUM.

    The Journal of experimental medicine·2009

    Area of Science:

    • Nephrology
    • Immunology
    • Pediatric Infectious Diseases

    Background:

    • Glomerulonephritis following pneumococcal infection is recognized.
    • The immunopathologic mechanisms remain incompletely understood.

    Purpose of the Study:

    • To explore the immunopathologic mechanisms of pneumococcal-associated glomerulonephritis.
    • To investigate complement system activation and kidney pathology in a pediatric case.

    Main Methods:

    • Serologic studies including complement component (C3, C4) levels.
    • Kidney biopsy analysis using light microscopy, immunofluorescence, and electron microscopy.
    • Detection of pneumococcal antigen and immune deposits in renal tissue.

    Main Results:

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    • Selective C3 hypocomplementemia developed during the disease course.
    • A serum factor degrading C3 was identified.
    • Kidney biopsy showed mesangial proliferative glomerulonephritis with glomerular-bound C3 and pneumococcal antigen.
    • Electron microscopy revealed subepithelial "humps" and intramembranous deposits.

    Conclusions:

    • Pneumococcal polysaccharides may activate the alternate complement pathway.
    • This activation likely contributes to the observed glomerulonephritis.
    • The findings suggest a mechanism for a limited course of pneumococcal-associated glomerulonephritis.