High RIPK3 expression is associated with a higher risk of early kidney transplant failure.
Molecular biology
Nephrology
Journal
iScience
ISSN: 2589-0042
Titre abrégé: iScience
Pays: United States
ID NLM: 101724038
Informations de publication
Date de publication:
20 Oct 2023
20 Oct 2023
Historique:
received:
02
07
2022
revised:
05
10
2022
accepted:
07
09
2023
medline:
23
10
2023
pubmed:
23
10
2023
entrez:
23
10
2023
Statut:
epublish
Résumé
Renal ischemia-reperfusion injury (IRI) is associated with reduced allograft survival, and each additional hour of cold ischemia time increases the risk of graft failure and mortality following renal transplantation. Receptor-interacting protein kinase 3 (RIPK3) is a key effector of necroptosis, a regulated form of cell death. Here, we evaluate the first-in-human RIPK3 expression dataset following IRI in kidney transplantation. The primary analysis included 374 baseline biopsy samples obtained from renal allografts 10 minutes after onset of reperfusion. RIPK3 was primarily detected in proximal tubular cells and distal tubular cells, both of which are affected by IRI. Time-to-event analysis revealed that high RIPK3 expression is associated with a significantly higher risk of one-year transplant failure and prognostic for one-year (death-censored) transplant failure independent of donor and recipient associated risk factors in multivariable analyses. The RIPK3 score also correlated with deceased donation, cold ischemia time and the extent of tubular injury.
Identifiants
pubmed: 37868627
doi: 10.1016/j.isci.2023.107879
pii: S2589-0042(23)01956-9
pmc: PMC10585402
doi:
Types de publication
Journal Article
Langues
eng
Pagination
107879Informations de copyright
© 2023 The Authors.
Déclaration de conflit d'intérêts
No author declares a conflict of interest.
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