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Related Experiment Videos

Terminal complement complexes in acute poststreptococcal glomerulonephritis

D G Matsell1, R J Wyatt, L W Gaber

  • 1Department of Pediatrics, University of Western Ontario, London, Canada.

Pediatric Nephrology (Berlin, Germany)
|December 1, 1994
PubMed
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Terminal complement complexes (TCC) activation is implicated in acute poststreptococcal glomerulonephritis (APSGN) pathogenesis. Local TCC generation, not urinary excretion, may drive glomerular injury in APSGN patients.

Area of Science:

  • Nephrology
  • Immunology
  • Pathology

Background:

  • Acute poststreptococcal glomerulonephritis (APSGN) involves complement cascade activation.
  • Terminal complement complexes (TCC) are formed during this activation process.

Purpose of the Study:

  • To investigate the role of TCC in the pathogenesis of glomerular injury in APSGN.
  • To assess TCC as a marker of disease activity in APSGN.

Main Methods:

  • Studied 30 patients diagnosed with APSGN.
  • Measured plasma concentrations of SC5b-9 and C3 over time.
  • Performed renal biopsies to examine C5b-9, S-protein, and C3 deposition.
  • Analyzed urinary TCC excretion during the acute phase.

Main Results:

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  • All patients exhibited elevated plasma SC5b-9 at nephritis onset.
  • Plasma SC5b-9 inversely correlated with time post-onset (r = -0.59), while C3 positively correlated (r = 0.78).
  • Renal biopsies showed glomerular deposition of C5b-9, S-protein, and C3.
  • Urinary TCC excretion was not elevated and did not correlate with disease activity.

Conclusions:

  • Terminal complement pathway activation occurs in APSGN.
  • Local generation of TCC likely contributes to glomerular injury in APSGN.
  • Urinary TCC is not a reliable marker for APSGN disease activity.