Circulating Levels of Endotrophin Are Prognostic for Long-Term Mortality after AKI.

AKI acute kidney injury and ICU nephrology basic science biomarker collagen type VI endotrophin fibrosis peptide fragments prognosis

Journal

Kidney360
ISSN: 2641-7650
Titre abrégé: Kidney360
Pays: United States
ID NLM: 101766381

Informations de publication

Date de publication:
26 05 2022
Historique:
received: 13 07 2021
accepted: 01 03 2022
entrez: 21 9 2022
pubmed: 22 9 2022
medline: 24 9 2022
Statut: epublish

Résumé

AKI involves a rapid decrease in kidney function that may be associated with structural damage. Early markers predicting AKI are emerging, but tools to assess patients' long-term health risks after AKI are still lacking. Endotrophin (ETP) is a bioactive molecule released during the formation of collagen type VI. We evaluated the potential of circulating ETP as a prognostic biomarker of adverse outcomes after AKI. We measured ETP in plasma samples collected 1 year after an episode of AKI, using the PRO-C6 ELISA in 801 patients (393 patients with AKI and 408 controls) from the prospective AKI Risk in Derby (ARID) study (ISRCTN25405995), who were then followed until year 3. Kidney disease progression was defined as ≥25% decline in eGFR combined with a decline in CKD stage. ETP levels were significantly higher in the AKI group compared with controls ( Patients in the AKI group had higher levels of plasma ETP at year 1 as compared with those who had not had AKI. In the AKI group, ETP levels predict kidney disease progression and mortality. Because ETP is a profibrotic molecule, our findings may indicate that ETP identifies patients with active fibrogenesis after AKI, suggestive of long-term renal remodeling, which is associated with patient outcome.

Sections du résumé

Background
AKI involves a rapid decrease in kidney function that may be associated with structural damage. Early markers predicting AKI are emerging, but tools to assess patients' long-term health risks after AKI are still lacking. Endotrophin (ETP) is a bioactive molecule released during the formation of collagen type VI. We evaluated the potential of circulating ETP as a prognostic biomarker of adverse outcomes after AKI.
Methods
We measured ETP in plasma samples collected 1 year after an episode of AKI, using the PRO-C6 ELISA in 801 patients (393 patients with AKI and 408 controls) from the prospective AKI Risk in Derby (ARID) study (ISRCTN25405995), who were then followed until year 3. Kidney disease progression was defined as ≥25% decline in eGFR combined with a decline in CKD stage.
Results
ETP levels were significantly higher in the AKI group compared with controls (
Conclusions
Patients in the AKI group had higher levels of plasma ETP at year 1 as compared with those who had not had AKI. In the AKI group, ETP levels predict kidney disease progression and mortality. Because ETP is a profibrotic molecule, our findings may indicate that ETP identifies patients with active fibrogenesis after AKI, suggestive of long-term renal remodeling, which is associated with patient outcome.

Identifiants

pubmed: 36128492
doi: 10.34067/KID.0000422021
pii: 02200512-202205000-00006
pmc: PMC9438419
doi:

Substances chimiques

Biomarkers 0
Collagen Type VI 0
Peptide Fragments 0
endotrophin 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

809-817

Informations de copyright

Copyright © 2022 by the American Society of Nephrology.

Déclaration de conflit d'intérêts

F. Genovese, M.A. Karsdal, and D.G.K. Rasmussen report being full-time employees at, and holding stock in, Nordic Bioscience. N. Sparding reports being a full-time employee at Nordic Bioscience and the University of Copenhagen. All remaining authors have nothing to disclose.

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Auteurs

Nadja Sparding (N)

Nordic Bioscience, Herlev, Denmark.
Biomedical Sciences, Faculty of Health and Medical Science, University of Copenhagen, Copenhagen, Denmark.

Daniel Guldager Kring Rasmussen (DGK)

Nordic Bioscience, Herlev, Denmark.

Federica Genovese (F)

Nordic Bioscience, Herlev, Denmark.

Morten Asser Karsdal (MA)

Nordic Bioscience, Herlev, Denmark.

Mads Hornum (M)

Department of Nephrology, Rigshospitalet, Copenhagen, Denmark.
Department of Clinical Medicine, University of Copenhagen, Copenhagen, Denmark.

Bo Feldt-Rasmussen (B)

Department of Nephrology, Rigshospitalet, Copenhagen, Denmark.
Department of Clinical Medicine, University of Copenhagen, Copenhagen, Denmark.

Rebecca Packington (R)

Centre for Kidney Research and Innovation, Academic Unit for Translational Medical Sciences, University of Nottingham, Nottingham, United Kingdom.

Nicholas M Selby (NM)

Centre for Kidney Research and Innovation, Academic Unit for Translational Medical Sciences, University of Nottingham, Nottingham, United Kingdom.
Department of Renal Medicine, University Hospitals of Derby and Burton, Derby, United Kingdom.

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