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

Mastellos, Dimitrios C.; Reis, Edimara S.; Biglarnia, Ali Reza LU ; Waldman, Meryl; Quigg, Richard J.; Huber-Lang, Markus; Seelen, Marc A.; Daha, Mohamed R. and Lambris, John D. (2019) In Clinical Immunology 198. p.102-105
Abstract

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... (More)

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.

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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
AMY-101, Complement C3, Compstatins, Cp40, Hemodialysis, Thromboinflammation
in
Clinical Immunology
volume
198
pages
102 - 105
publisher
Elsevier
external identifiers
  • scopus:85057279543
ISSN
1521-6616
DOI
10.1016/j.clim.2018.11.010
language
English
LU publication?
yes
id
f16f6e07-e3fc-458b-a16e-0aff8e47b8c9
date added to LUP
2018-12-04 13:47:41
date last changed
2019-09-17 04:45:01
@article{f16f6e07-e3fc-458b-a16e-0aff8e47b8c9,
  abstract     = {<p>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.</p>},
  author       = {Mastellos, Dimitrios C. and Reis, Edimara S. and Biglarnia, Ali Reza and Waldman, Meryl and Quigg, Richard J. and Huber-Lang, Markus and Seelen, Marc A. and Daha, Mohamed R. and Lambris, John D.},
  issn         = {1521-6616},
  keyword      = {AMY-101,Complement C3,Compstatins,Cp40,Hemodialysis,Thromboinflammation},
  language     = {eng},
  pages        = {102--105},
  publisher    = {Elsevier},
  series       = {Clinical Immunology},
  title        = {Taming hemodialysis-induced inflammation : Are complement C3 inhibitors a viable option?},
  url          = {http://dx.doi.org/10.1016/j.clim.2018.11.010},
  volume       = {198},
  year         = {2019},
}