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Related Experiment Video

Updated: May 13, 2026

Analyses of Proteinuria, Renal Infiltration of Leukocytes, and Renal Deposition of Proteins in Lupus-prone MRL/lpr Mice
09:43

Analyses of Proteinuria, Renal Infiltration of Leukocytes, and Renal Deposition of Proteins in Lupus-prone MRL/lpr Mice

Published on: June 8, 2022

Complement and kidney disease.

H Terence Cook1

  • 1Department of Medicine, Centre for Complement and Inflammation Research, Imperial College London, London, UK.

Current Opinion in Nephrology and Hypertension
|March 20, 2013
PubMed
Summary
This summary is machine-generated.

Genetic variations in the complement system are increasingly linked to kidney diseases like IgA nephropathy and lupus. New therapies targeting complement activation show promise for treating these renal pathologies.

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Area of Science:

  • Nephrology
  • Immunology
  • Genetics

Background:

  • The complement system is a crucial part of innate immunity.
  • Dysregulation of the complement system is implicated in various kidney diseases.
  • Genetic factors play a significant role in complement-mediated renal pathology.

Purpose of the Study:

  • To review recent findings on the complement system's role in renal pathology.
  • To highlight the association between genetic variations and kidney diseases.
  • To discuss emerging therapeutic strategies targeting the complement system.

Main Methods:

  • Review of recent literature on complement system and renal pathology.
  • Analysis of genetic association studies (GWAS) and mutation analyses.
  • Examination of preclinical and clinical studies of complement-targeted therapies.

Main Results:

  • Genetic variations in complement and its control proteins are linked to IgA nephropathy, systemic lupus erythematosus (SLE), C3 glomerulopathy, and hemolytic uremic syndrome.
  • Polymorphisms in complement factor H-related genes are associated with susceptibility to IgA nephropathy and SLE.
  • Mutations in complement genes are linked to familial C3 glomerulopathy and hemolytic uremic syndrome.
  • Anti-C5 antibody therapy is being explored for renal diseases.
  • Targeted inhibition of C3 activation shows promise in preclinical models.

Conclusions:

  • Complement activation and dysregulation are key factors in diverse renal pathologies.
  • Emerging therapeutic strategies offer potential for targeted treatment of complement-mediated kidney diseases.