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Intradialytic Complement Activation Precedes the Development of Cardiovascular Events in Hemodialysis Patients

2018Journal article Open access
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dc.contributor.authorPoppelaars, F
dc.contributor.authorGaya da Costa, M
dc.contributor.authorFaria, B
dc.contributor.authorBerger, SP
dc.contributor.authorAssa, S
dc.contributor.authorDaha, MR
dc.contributor.authorMedina Pestana, JO
dc.contributor.authorvan Son, WJ
dc.contributor.authorFranssen, CF
dc.contributor.authorSeelen, MA
dc.date.accessioned2019-01-18T16:04:14Z
dc.date.available2019-01-18T16:04:14Z
dc.date.issued2018
dc.description.abstractBackground: Hemodialysis (HD) is a life-saving treatment for patients with end stage renal disease. However, HD patients have markedly increased rates of cardiovascular morbidity and mortality. Previously, a link between the complement system and cardiovascular events (CV-events) has been reported. In HD, systemic complement activation occurs due to blood-to-membrane interaction. We hypothesize that HD-induced complement activation together with inflammation and thrombosis are involved in the development of CV-events in these patients. Methods: HD patients were followed for the occurrence of CV-events during a maximum follow-up of 45 months. Plasma samples were collected from 55 patients at different time points during one HD session prior to follow-up. Plasma levels of mannose-binding lectin, properdin and C3d/C3 ratios were assessed by ELISA. In addition, levels of von Willebrand factor, TNF-α and IL-6/IL-10 ratios were determined. An ex-vivo model of HD was used to assess the effect of complement inhibition. Results: During median follow-up of 32 months, 17 participants developed CV-events. In the CV-event group, the C3d/C3-ratio sharply increased 30 min after the start of the HD session, while in the event-free group the ratio did not increase. In accordance, HD patients that developed a CV-event also had a sustained higher IL-6/IL-10-ratio during the first 60 min of the HD session, followed by a greater rise in TNF-α levels and von Willebrand factor at the end of the session. In the ex-vivo HD model, we found that complement activation contributed to the induction of TNF-α levels, IL-6/IL-10-ratio and levels of von Willebrand factor. Conclusions: In conclusion, these findings suggest that early intradialytic complement activation predominantly occurred in HD patients who develop a CV-event during follow-up. In addition, in these patients complement activation was accompanied by a pro-inflammatory and pro-thrombotic response. Experimental complement inhibition revealed that this reaction is secondary to complement activation. Therefore, our data suggests that HD-induced complement, inflammation and coagulation are involved in the increased CV risk of HD patients.pt_PT
dc.description.versioninfo:eu-repo/semantics/publishedVersionpt_PT
dc.identifier.citationFront Immunol. 2018 Sep 13;9:2070.pt_PT
dc.identifier.doi10.3389/fimmu.2018.02070pt_PT
dc.identifier.urihttp://hdl.handle.net/10400.23/1304
dc.language.isoengpt_PT
dc.peerreviewedyespt_PT
dc.subjectDoenças Cardiovascularespt_PT
dc.subjectDiálise Renalpt_PT
dc.titleIntradialytic Complement Activation Precedes the Development of Cardiovascular Events in Hemodialysis Patientspt_PT
dc.typejournal article
dspace.entity.typePublication
oaire.citation.startPage2070pt_PT
oaire.citation.volume9pt_PT
rcaap.rightsopenAccesspt_PT
rcaap.typearticlept_PT

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