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The complement system is a group of approximately 20 plasma proteins that strengthen the body's defenses against infections through opsonization, inflammation, and cell lysis. Opsonization involves coating pathogens with complement proteins, making them more recognizable and facilitating phagocyte engulfment. Certain complement proteins induce inflammation that attracts immune cells to the site of infection. Cell lysis involves the destruction of pathogens through the formation of a...
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Related Experiment Video

Updated: Dec 2, 2025

Analyses of Proteinuria, Renal Infiltration of Leukocytes, and Renal Deposition of Proteins in Lupus-prone MRL/lpr Mice
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Is primary membranous nephropathy a complement mediated disease?

Linda Reinhard1, Rolf A K Stahl1, Elion Hoxha1

  • 1III. Department of Medicine, University Medical Center Hamburg-Eppendorf, Martinistrasse 52, 20246, Hamburg, Germany.

Molecular Immunology
|November 3, 2020
PubMed
Summary

Membranous nephropathy involves immune complexes damaging kidney podocytes. This review clarifies the complement system's role in primary membranous nephropathy pathogenesis, focusing on autoantigens like PLA2R.

Keywords:
AutoimmunityComplementIgG4 antibody subclassKidney diseaseMembranous nephropathy

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Area of Science:

  • Nephrology
  • Immunology
  • Pathophysiology

Background:

  • Membranous nephropathy (MN) is an immune complex-mediated kidney disease.
  • Primary MN involves autoantibodies targeting glomerular podocyte antigens.
  • Complement system activation is implicated in MN pathogenesis.

Purpose of the Study:

  • To review current knowledge on the complement system's function in primary MN.
  • To discuss unresolved questions regarding complement's role in MN pathophysiology.

Main Methods:

  • Literature review of existing clinical and experimental evidence.
  • Focus on recent discoveries of podocyte autoantigens (PLA2R, THSD7A).

Main Results:

  • Immune deposits activate the complement system.
  • Terminal complement complex (MAC) may disrupt the glomerular filtration barrier.
  • IgG4 autoantibodies against PLA2R and THSD7A are implicated in >85% of primary MN cases.

Conclusions:

  • The precise role of complement in primary MN pathogenesis requires further definition.
  • Understanding complement's contribution is crucial for advancing MN pathophysiology knowledge.