Complement activation in progressive renal disease
Open Access
- 1 January 2015
- journal article
- review article
- Published by Baishideng Publishing Group Inc. in World Journal of Nephrology
- Vol. 4 (1), 31-40
- https://doi.org/10.5527/wjn.v4.i1.31
Abstract
Chronic kidney disease (CKD) is common and the cause of significant morbidity and mortality. The replacement of functioning nephrons by fibrosis is characteristic of progressive disease. The pathways that lead to fibrosis are not fully understood, although chronic non-resolving inflammation in the kidney is likely to drive the fibrotic response that occurs. In patients with progressive CKD there is histological evidence of inflammation in the interstitium and strategies that reduce inflammation reduce renal injury in pre-clinical models of CKD. The complement system is an integral part of the innate immune system but also augments adaptive immune responses. Complement activation is known to occur in many diverse renal diseases, including glomerulonephritis, thrombotic microangiopathies and transplant rejection. In this review we discuss current evidence that complement activation contributes to progression of CKD, how complement could cause renal inflammation and whether complement inhibition would slow progression of renal disease.Keywords
This publication has 93 references indexed in Scilit:
- Urine proteome of autosomal dominant polycystic kidney disease patientsClinical Proteomics, 2012
- Mannan-Binding Lectin in Diabetic Kidney Disease: The Impact of Mouse Genetics in a Type 1 Diabetes ModelExperimental Diabetes Research, 2012
- Transcriptome Analysis of Human Diabetic Kidney DiseaseDiabetes, 2011
- Identification of Tubular Heparan Sulfate as a Docking Platform for the Alternative Complement Component Properdin in Proteinuric Renal DiseaseJournal of Biological Chemistry, 2011
- Expression of Complement Components Differs Between Kidney Allografts from Living and Deceased DonorsJournal of the American Society of Nephrology, 2009
- Elevated MBL Concentrations Are Not an Indication of Association Between the MBL2 Gene and Type 1 Diabetes or Diabetic NephropathyDiabetes, 2009
- Systems biology of autosomal dominant polycystic kidney disease (ADPKD): computational identification of gene expression pathways and integrated regulatory networksHuman Molecular Genetics, 2009
- C3a Mediates Epithelial-to-Mesenchymal Transition in Proteinuric NephropathyJournal of the American Society of Nephrology, 2009
- Characterization of the renal cyst fluid proteome in autosomal dominant polycystic kidney disease (ADPKD) patientsProteomics – Clinical Applications, 2008
- Chronic kidney disease management in the United Kingdom: NEOERICA project resultsKidney International, 2007