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Complement activation in acute glomerulonephritis in children.

M Levy, M Sich, E Pirotzky

    The International Journal of Pediatric Nephrology
    |January 1, 1985
    PubMed
    Summary
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    This study in children with acute glomerulonephritis found low complement component C3 levels in most patients, suggesting both classical and alternative complement pathways are involved in the early disease stages.

    Area of Science:

    • Immunology
    • Nephrology
    • Pediatrics

    Background:

    • Acute glomerulonephritis is an inflammatory kidney disease.
    • Complement system activation plays a role in glomerulonephritis pathogenesis.

    Purpose of the Study:

    • To investigate the role of complement pathways in acute glomerulonephritis in children.
    • To analyze serial changes in complement components during the disease course.

    Main Methods:

    • Serial measurements of complement components (C1q, C4, C3, C5, Factor B) in 32 children.
    • Assay for C3 splitting activity and C3 nephritic factor-like activity.

    Main Results:

    • Low C3 levels observed in 30/32 patients; low C5 in 26/32.
    • Reduced C1q/C4 in 25 patients suggested classical pathway activation.

    Related Experiment Videos

  • C3 splitting and/or C3 nephritic factor-like activities detected in 8 patients, disappearing over time.
  • Heat-labile C3 nephritic factor-like activity identified in 3 patients.

    • Conclusions:

    • Both classical and alternative complement pathways are implicated in early acute glomerulonephritis.
    • Continued C3 depression likely mediated by the alternative pathway.
    • Transient C3 nephritic factor-like activity may contribute to disease pathogenesis.