Taming hemodialysis-induced inflammation: Are complement C3 inhibitors a viable option?

Research output: Contribution to journalArticle


Owing to an increasing shortage of donor organs, the majority of patients with end-stage kidney disease remains reliant on extracorporeal hemodialysis (HD) in order to counter the lifelong complications of a failing kidney. While HD remains a life-saving option for these patients, mounting evidence suggests that it also fuels a vicious cycle of thromboinflammation that can increase the risk of cardiovascular disease. During HD, blood-borne innate immune systems become inappropriately activated on the biomaterial surface, instigating proinflammatory reactions that can alter endothelial and vascular homeostasis. Complement activation, early during the HD process, has been shown to fuel a multitude of detrimental thromboinflammatory reactions that collectively contribute to patient morbidity. Here we discuss emerging aspects of complement's involvement in HD-induced inflammation and put forth the concept that targeted intervention at the level of C3 might constitute a promising therapeutic approach in HD patients.


  • Dimitrios C. Mastellos
  • Edimara S. Reis
  • Ali Reza Biglarnia
  • Meryl Waldman
  • Richard J. Quigg
  • Markus Huber-Lang
  • Marc A. Seelen
  • Mohamed R. Daha
  • John D. Lambris
External organisations
  • National Centre for Scientific Research Demokritos
  • University of Pennsylvania
  • National Institutes of Health, United States
  • University at Buffalo
  • University Hospital of Ulm
  • University Medical Center Groningen
  • Leiden University Medical Centre
  • Skåne University Hospital
Research areas and keywords

Subject classification (UKÄ) – MANDATORY

  • Urology and Nephrology


  • AMY-101, Complement C3, Compstatins, Cp40, Hemodialysis, Thromboinflammation
Original languageEnglish
Pages (from-to)102-105
JournalClinical Immunology
Early online date2018 Nov 22
Publication statusPublished - 2019
Publication categoryResearch