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Related Experiment Videos

Complement depletion abolishes IgA-mediated glomerular inflammation in rats

R K Stad1, D J van Gijlswijk-Janssen, L A van Es

  • 1Department of Nephrology, University Hospital Leiden, The Netherlands.

Experimental Nephrology
|May 1, 1994
PubMed
Summary
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Human IgA activates the complement system via the mannan-binding lectin pathway.

Journal of immunology (Baltimore, Md. : 1950)·2001

Complement activation is crucial for IgA-mediated glomerular inflammation and proteinuria in rats. Depleting complement prevents proteinuria despite IgA deposition and macrophage influx.

Area of Science:

  • Nephrology
  • Immunology
  • Pathology

Background:

  • Polymeric IgA immune complexes induce acute glomerular inflammation in rats.
  • This inflammation involves complement activation, macrophages, and proteinuria.

Purpose of the Study:

  • To investigate the role of complement (C) in IgA-mediated nephritis.
  • To determine if complement depletion affects IgA-induced glomerular inflammation and proteinuria.

Main Methods:

  • Rats were depleted of C3 using cobra venom factor (CVF) or received a placebo.
  • Mesangial IgA deposits were introduced.
  • Proteinuria, glomerular C3/C9 deposition, and macrophage influx were analyzed.

Main Results:

  • Proteinuria occurred only in normocomplementemic rats with IgA deposits.

Related Experiment Videos

  • C3 and C9 deposition colocalized with IgA in normocomplementemic rats, but not in C-depleted rats.
  • Macrophage influx occurred in both groups, but proteinuria was absent in C-depleted rats.

    • Conclusions:

    • Complement activation via the alternative pathway is essential for IgA-mediated proteinuria.
    • While IgA deposition and macrophage influx occur without complement, proteinuria requires complement activation.