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Related Experiment Videos

The alternative pathway C3 convertase and glomerular deposits.

C D West1, A J McAdams

  • 1Division of Nephrology, Children's Hospital Medical Center, Cincinnati, OH 45229-3039, USA.

Pediatric Nephrology (Berlin, Germany)
|July 21, 1999
PubMed
Summary

Excess complement C3 convertase, C3b,Bb, due to factor H dysfunction causes nephritis. This occurs in Marder disease, factor H deficiency, and specific types of membranoproliferative glomerulonephritis (MPGN).

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Area of Science:

  • Immunology
  • Nephrology
  • Complement System Biology

Background:

  • Factor H dysfunction leads to excess alternative pathway C3 convertase (C3b,Bb), frequently causing nephritis.
  • This condition is observed in Marder disease (factor H binding site defect), homozygous factor H deficiency, factor H inhibitors, and specific MPGN types.

Purpose of the Study:

  • To investigate the relationship between excess complement convertase and glomerular deposits in various nephritic conditions.
  • To analyze the correlation between complement levels and the presence/type of glomerular deposits in MPGN types II and III, factor H deficiency, and Marder disease.

Main Methods:

  • Observational study analyzing clinical data and biopsy findings.
  • Correlation of complement levels (hypocomplementemic vs. normocomplementemic) with the presence and location of glomerular deposits.

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Main Results:

  • In MPGN type II, subepithelial paramesangial deposits correlate with hypocomplementemia.
  • MPGN type III shows paramesangial deposits with hypocomplementemia and subendothelial deposits only during hypocomplementemia.
  • Paramesangial deposits are characteristic of factor H deficiency and Marder disease.

Conclusions:

  • Excessive C3 convertase is linked to nephritis and specific glomerular deposition patterns.
  • Variations in nephritis incidence, severity, and morphology may depend on convertase characteristics and C3 products.