Complement and kidney disease

Curr Opin Nephrol Hypertens. 2013 May;22(3):295-301. doi: 10.1097/MNH.0b013e32835ff9cb.


Purpose of review: This review summarizes recent key findings relating to the role of the complement system in renal pathology.

Recent findings: There is increasing association of genetic variations in complement and complement control proteins with renal disease. Genome-wide association studies have shown that polymorphisms at the complement factor H-related gene locus are associated with susceptibility to IgA nephropathy and systemic lupus erythematosus (SLE). Rare mutations in these genes are associated with familial forms of C3 glomerulopathy. Mutations in other complement genes have been associated with C3 glomerulopathy and hemolytic uremic syndrome. There are now several reports of the use of anti-C5 antibody therapy in renal disease. Preclinical studies have shown the utility of targeted inhibition of C3 activation in models of lupus glomerulonephritis and ischemia reperfusion injury.

Summary: Complement activation or dysregulation is important in a range of renal pathology and new therapeutic strategies are being developed which may allow rational therapy for these diseases.

Publication types

  • Review

MeSH terms

  • Animals
  • Antibodies, Monoclonal, Humanized / therapeutic use
  • Complement Activation* / drug effects
  • Complement Activation* / genetics
  • Complement Inactivating Agents / therapeutic use
  • Complement System Proteins / genetics
  • Complement System Proteins / metabolism*
  • Genetic Predisposition to Disease
  • Humans
  • Kidney / drug effects
  • Kidney / immunology*
  • Kidney / pathology
  • Kidney Diseases / drug therapy
  • Kidney Diseases / genetics
  • Kidney Diseases / immunology*
  • Kidney Diseases / pathology
  • Mutation
  • Phenotype
  • Risk Factors
  • Treatment Outcome


  • Antibodies, Monoclonal, Humanized
  • Complement Inactivating Agents
  • Complement System Proteins
  • eculizumab