Temporal changes in complement activation in haemodialysis patients with COVID-19 as a predictor of disease progression.

COVID-19 complement haemodialysis

Journal

Clinical kidney journal
ISSN: 2048-8505
Titre abrégé: Clin Kidney J
Pays: England
ID NLM: 101579321

Informations de publication

Date de publication:
Oct 2020
Historique:
received: 11 08 2020
accepted: 27 08 2020
entrez: 30 10 2020
pubmed: 31 10 2020
medline: 31 10 2020
Statut: epublish

Résumé

Complement activation may play a pathogenic role in patients with severe coronavirus disease 2019 (COVID-19) by contributing to tissue inflammation and microvascular thrombosis. Serial samples were collected from patients receiving maintenance haemodialysis (HD). Thirty-nine patients had confirmed COVID-19 and 10 patients had no evidence of COVID-19. Plasma C5a and C3a levels were measured using enzyme-linked immunosorbent assay. We identified elevated levels of plasma C3a and C5a in HD patients with severe COVID-19 compared with controls. Serial sampling identified that C5a levels were elevated prior to clinical deterioration in patients who developed severe disease. C3a more closely mirrored both clinical and biochemical disease severity. Our findings suggest that activation of complement plays a role in the pathogenesis of COVID-19, leading to endothelial injury and lung damage. C5a may be an earlier biomarker of disease severity than conventional parameters such as C-reactive protein and this warrants further investigation in dedicated biomarker studies. Our data support the testing of complement inhibition as a therapeutic strategy for patients with severe COVID-19.

Sections du résumé

BACKGROUND BACKGROUND
Complement activation may play a pathogenic role in patients with severe coronavirus disease 2019 (COVID-19) by contributing to tissue inflammation and microvascular thrombosis.
METHODS METHODS
Serial samples were collected from patients receiving maintenance haemodialysis (HD). Thirty-nine patients had confirmed COVID-19 and 10 patients had no evidence of COVID-19. Plasma C5a and C3a levels were measured using enzyme-linked immunosorbent assay.
RESULTS RESULTS
We identified elevated levels of plasma C3a and C5a in HD patients with severe COVID-19 compared with controls. Serial sampling identified that C5a levels were elevated prior to clinical deterioration in patients who developed severe disease. C3a more closely mirrored both clinical and biochemical disease severity.
CONCLUSIONS CONCLUSIONS
Our findings suggest that activation of complement plays a role in the pathogenesis of COVID-19, leading to endothelial injury and lung damage. C5a may be an earlier biomarker of disease severity than conventional parameters such as C-reactive protein and this warrants further investigation in dedicated biomarker studies. Our data support the testing of complement inhibition as a therapeutic strategy for patients with severe COVID-19.

Identifiants

pubmed: 33123364
doi: 10.1093/ckj/sfaa192
pii: sfaa192
pmc: PMC7577776
doi:

Types de publication

Journal Article

Langues

eng

Pagination

889-896

Subventions

Organisme : Wellcome Trust
Pays : United Kingdom
Organisme : Wellcome Trust
ID : 212252/Z/18/Z
Pays : United Kingdom
Organisme : Medical Research Council
ID : MR/S004068/2
Pays : United Kingdom

Informations de copyright

© The Author(s) 2020. Published by Oxford University Press on behalf of ERA-EDTA.

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Auteurs

Maria Prendecki (M)

Centre for Inflammatory Disease, Imperial College London, London, UK.

Candice Clarke (C)

Centre for Inflammatory Disease, Imperial College London, London, UK.

Nicholas Medjeral-Thomas (N)

Centre for Inflammatory Disease, Imperial College London, London, UK.

Stephen P McAdoo (SP)

Centre for Inflammatory Disease, Imperial College London, London, UK.

Eleanor Sandhu (E)

Centre for Inflammatory Disease, Imperial College London, London, UK.

James E Peters (JE)

Centre for Inflammatory Disease, Imperial College London, London, UK.
Health Data Research UK, London, UK.

David C Thomas (DC)

Centre for Inflammatory Disease, Imperial College London, London, UK.

Michelle Willicombe (M)

Centre for Inflammatory Disease, Imperial College London, London, UK.

Marina Botto (M)

Centre for Inflammatory Disease, Imperial College London, London, UK.

Matthew C Pickering (MC)

Centre for Inflammatory Disease, Imperial College London, London, UK.

Classifications MeSH