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Complement System01:27

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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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The glomerulus and Bowman's capsule are two essential components of the nephron, which is the functional unit of the kidney. These microscopic structures play a critical role in the process of blood filtration to produce urine.
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[Retinopathy associated with thrombotic microangiopathy of mixed origin (case report)].

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Related Experiment Video

Updated: Feb 25, 2026

Analyses of Proteinuria, Renal Infiltration of Leukocytes, and Renal Deposition of Proteins in Lupus-prone MRL/lpr Mice
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[Changes in the complement system in membranoproliferative glomerulonephritis].

V A Yurova1, L A Bobrova1, N L Kozlovskaya1

  • 1I.M. Sechenov First Moscow State Medical University, Ministry of Health of Russia, Moscow, Russia.

Terapevticheskii Arkhiv
|July 27, 2017
PubMed
Summary

This study compared membranoproliferative glomerulonephritis (MPGN) variants, finding C3 glomerulopathy (C3-GP) involves alternative complement pathway dysregulation. C3-GP patients showed distinct complement levels, highlighting its role in pathogenesis.

Keywords:
C3 glomerulopathyC3 nephritic factoralternative complement pathwaycomplement dysregulationdense deposit diseasemembranoproliferative glomerulonephritis

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Area of Science:

  • Nephrology
  • Immunology
  • Complement System Biology

Background:

  • Membranoproliferative glomerulonephritis (MPGN) encompasses diverse conditions.
  • Lupus nephritis (LN) and C3 glomerulopathy (C3-GP) are distinct MPGN subtypes.
  • Complement system activation is implicated in MPGN pathogenesis.

Purpose of the Study:

  • To compare clinical and complement system features of idiopathic MPGN, Class IV LN, and C3-GP.
  • To elucidate the role of complement dysregulation in C3-GP pathogenesis.

Main Methods:

  • Retrospective analysis of 42 MPGN patients (2013-2015).
  • Included 35 patients: 8 C3-GP, 13 idiopathic MPGN, 14 Class IV LN.
  • Assessed blood/urine complement components (C3, C4, C3a, C5a, CFH, CFB, CFD) and terminal complement complex (TCC) activation markers.

Main Results:

  • C3-GP detected in 19% of MPGN cases.
  • C3-GP patients exhibited lowest serum C3 and highest urinary C3a, C5a, TCC, CFH, CFB, and CFD.
  • C3 nephritic factor found in 2 C3-GP patients (dense deposit disease).

Conclusions:

  • Alternative complement pathway dysregulation is central to C3-GP pathogenesis.
  • Genetic or autoimmune factors likely drive this dysregulation in C3-GP.