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High RIPK3 expression is associated with a higher risk of early kidney transplant failure
A. Wahida, C. Schmaderer, M. Büttner-Herold, C. Branca, S. Donakonda, F. Haberfellner, C. Torrez, J. Schmitz, T. Schulze, T. Seibt, R. Öllinger, T. Engleitner, B. Haller, K. Steiger, R. Günthner, G. Lorenz, M. Yabal, Q. Bachmann, MC. Braunisch,...
Status neindexováno Jazyk angličtina Země Spojené státy americké
Typ dokumentu časopisecké články
PubMed Central od 2018
Europe PubMed Central od 2018
Elsevier Open Access Journals od 2018-03-23
ROAD: Directory of Open Access Scholarly Resources od 2018
Odkazy
PubMed
37868627
DOI
10.1016/j.isci.2023.107879
Knihovny.cz E-zdroje
- Publikační typ
- časopisecké články MeSH
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.
CECAD University of Cologne Faculty of Medicine and University Hospital Cologne Cologne Germany
Department of General Visceral and Cancer Surgery University of Cologne Cologne Germany
Department of Immunology St Jude Children's Research Hospital Memphis TN USA
Department of Nephropathology Friedrich Alexander University Erlangen Nurnberg Erlangen Germany
Department of Surgery Klinikum rechts der Isar Technical University of Munich Munich Germany
Division of Nephrology Department of Medicine Albert Einstein College of Medicine Bronx NY USA
Institute of Pathology TUM School of Medicine Technical University of Munich Munich Germany
Nephropathology Unit Institute of Pathology Hannover Medical School Hannover Germany
Transplant Center University Hospital Munich Ludwig Maximilians University Munich Germany
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- $a 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.
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