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


Journal

Clinical immunology (Orlando, Fla.)
ISSN: 1521-7035
Titre abrégé: Clin Immunol
Pays: United States
ID NLM: 100883537

Informations de publication

Date de publication:
01 2019
Historique:
received: 09 11 2018
accepted: 19 11 2018
pubmed: 26 11 2018
medline: 29 10 2019
entrez: 26 11 2018
Statut: ppublish

Résumé

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.

Identifiants

pubmed: 30472267
pii: S1521-6616(18)30648-X
doi: 10.1016/j.clim.2018.11.010
pmc: PMC7366512
mid: NIHMS1605321
pii:
doi:

Substances chimiques

Complement C3 0
Complement Inactivating Agents 0

Types de publication

Journal Article Research Support, N.I.H., Extramural

Langues

eng

Sous-ensembles de citation

IM

Pagination

102-105

Subventions

Organisme : NIAID NIH HHS
ID : N01 AI030040
Pays : United States
Organisme : NIAID NIH HHS
ID : P01 AI068730
Pays : United States
Organisme : NIAID NIH HHS
ID : R01 AI030040
Pays : United States

Informations de copyright

Published by Elsevier Inc.

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Auteurs

Dimitrios C Mastellos (DC)

Division of Biodiagnostic Sciences and Technologies, National Center for Scientific Research 'Demokritos', Athens, Greece.

Edimara S Reis (ES)

Department of Pathology and Laboratory Medicine, Perelman School of Medicine, University of Pennsylvania, USA.

Ali-Reza Biglarnia (AR)

Department of Transplantation, Skåne University Hospital, Malmö, Lund University, Lund, Sweden.

Meryl Waldman (M)

Kidney Disease Section, Kidney Diseases Branch, NIH, Bethesda, USA.

Richard J Quigg (RJ)

Division of Nephrology, Department of Medicine, Jacobs School of Medicine & Biomedical Sciences, University at Buffalo, USA.

Markus Huber-Lang (M)

Institute for Clinical and Experimental Trauma-Immunology, University Hospital of Ulm, Ulm, Germany.

Marc A Seelen (MA)

Division of Nephrology, Department of Internal Medicine, University of Groningen, University Medical Center Groningen, Groningen, Netherlands.

Mohamed R Daha (MR)

Department of Nephrology, Leiden University Medical Centre, Leiden, Netherlands.

John D Lambris (JD)

Department of Pathology and Laboratory Medicine, Perelman School of Medicine, University of Pennsylvania, USA. Electronic address: lambris@pennmedicine.upenn.edu.

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