Prolonged cold ischemia accelerates cellular and humoral chronic rejection in a rat model of kidney allotransplantation

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dc.contributor.authorSolini, Samantha
dc.contributor.authorAiello, Sistiana
dc.contributor.authorCassis, Paola
dc.contributor.authorScudeletti, Pierangela
dc.contributor.authorAzzollini, Nadia
dc.contributor.authorMister, Marilena
dc.contributor.authorRocchetta, Federica
dc.contributor.authorAbbate, Mauro
dc.contributor.authorPereira, Rafael Luiz [UNIFESP]
dc.contributor.authorNoris, Marina
dc.contributor.institutionMario Negri Inst Pharmacol Res
dc.contributor.institutionCtr Anna Maria Astori
dc.contributor.institutionUniversidade Federal de São Paulo (UNIFESP)
dc.date.accessioned2016-01-24T14:17:56Z
dc.date.available2016-01-24T14:17:56Z
dc.date.issued2012-03-01
dc.description.abstractOne of the leading causes of long-term kidney graft loss is chronic allograft injury (CAI), a pathological process triggered by alloantigen-dependent and alloantigen-independent factors. Alloantigen-independent factors, such as cold ischemia (CI) may amplify the recipient immune response against the graft. We investigated the impact of prolonged cold ischemia and the subsequent delayed graft function on CAI in a fully MHC-mismatched rat model of kidney allotransplantation. Prolonged CI was associated with anticipation of proteinuria onset and graft function deterioration (ischemia: 90d; no ischemia: 150d), more severe tubular atrophy, interstitial fibrosis, and glomerulosclerosis, and increased mortality rate (180d survival, ischemia: 0%; no ischemia: 67%). in ischemic allografts, T and B cells were detected very early and were organized in inflammatory clusters. Higher expression of BAFF-R and TACI within the ischemic allografts indicates that B cells are mature and activated. As a consequence of B cell activity, anti-donor antibodies, glomerular C4d and IgG deposition, important features of chronic humoral rejection, appeared earlier in ischemic than in non-ischemic allograft recipients. Thus, prolonged CI time plays a main role in CAI development by triggering acceleration of cellular and humoral reactions of chronic rejection. Limiting CI time should be considered as a main target in kidney transplantation.en
dc.description.affiliationMario Negri Inst Pharmacol Res, Transplant Res Ctr, I-24020 Ranica, Bergamo, Italy
dc.description.affiliationCtr Anna Maria Astori, Mario Negri Inst Pharmacol Res, Bergamo, Italy
dc.description.affiliationUniversidade Federal de São Paulo, Disciplina Nefrol, Lab Imunol Clin & Expt, Dept Med, São Paulo, Brazil
dc.description.affiliationUnifespUniversidade Federal de São Paulo, Disciplina Nefrol, Lab Imunol Clin & Expt, Dept Med, São Paulo, Brazil
dc.description.sourceWeb of Science
dc.description.sponsorshipFondazione ART per la Ricerca sui Trapianti ONLUS (ART, Milan, Italy)
dc.description.sponsorshipFondazione ART per la Ricerca sui Trapianti, Milano
dc.description.sponsorshipConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.description.sponsorshipIDCNPq: 3093107
dc.format.extent347-356
dc.identifierhttp://dx.doi.org/10.1111/j.1432-2277.2011.01425.x
dc.identifier.citationTransplant International. Malden: Wiley-Blackwell, v. 25, n. 3, p. 347-356, 2012.
dc.identifier.doi10.1111/j.1432-2277.2011.01425.x
dc.identifier.issn0934-0874
dc.identifier.urihttp://repositorio.unifesp.br/handle/11600/34641
dc.identifier.wosWOS:000299924900018
dc.language.isoeng
dc.publisherWiley-Blackwell
dc.relation.ispartofTransplant International
dc.rightsinfo:eu-repo/semantics/openAccess
dc.rights.licensehttp://olabout.wiley.com/WileyCDA/Section/id-406071.html
dc.subjectchronic allograft injuryen
dc.subjectischemiaen
dc.subjectreperfusionen
dc.subjectkidney transplanten
dc.titleProlonged cold ischemia accelerates cellular and humoral chronic rejection in a rat model of kidney allotransplantationen
dc.typeinfo:eu-repo/semantics/article
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