Acute Kidney Injury Following Chimeric Antigen Receptor T-Cell Therapy for B-Cell Lymphoma in a Kidney Transplant Recipient

dc.contributor.authorMelilli, Edoardo
dc.contributor.authorMussetti, Alberto
dc.contributor.authorSanz Linares, Gabriela
dc.contributor.authorRuella, Marco
dc.contributor.authorLa Salette, Charette
dc.contributor.authorSavchenko, Alexandre
dc.contributor.authorTaco, Rosario
dc.contributor.authorMontero, Nuria
dc.contributor.authorGrinyó Boira, Josep M.
dc.contributor.authorFavà Buch, Alexandre
dc.contributor.authorGomà, Montse
dc.contributor.authorMeneghini, Maria
dc.contributor.authorManonelles, Anna
dc.contributor.authorCruzado, Josep Ma.
dc.contributor.authorSureda, Anna
dc.contributor.authorBestard Matamoros, Oriol
dc.date.accessioned2021-09-13T09:46:50Z
dc.date.available2021-09-13T09:46:50Z
dc.date.issued2021-07-01
dc.date.updated2021-09-10T08:43:52Z
dc.description.abstractAnti-CD19 chimeric antigen receptor (CAR) T-cell therapy is a newer and effective therapeutic option approved for patients with relapsed/refractory acute lymphoblastic leukemia and diffuse large B-cell lymphoma. Acute kidney injury is a complication of CAR T-cell therapy that can result in kidney failure. In most cases, it is thought to be related to hemodynamic changes due to cytokine release syndrome. Kidney biopsy in this clinical scenario is usually not performed. We report on a kidney transplant recipient in his 40s who developed a posttransplant lymphoproliferative disorder of B-cell origin refractory to conventional treatments and received anti-CD19 CAR T-cell therapy as compassionate treatment. Beginning on day 12 after CAR T-cell infusion, in the absence of clinical symptoms, a progressive decline in estimated glomerular filtration rate of the kidney graft occurred. A subsequent allograft biopsy showed mild tubulointerstitial lymphocyte infiltrates, falling into a Banff borderline-changes category and resembling an acute immunoallergic tubulointerstitial nephritis. Neither CAR T cells nor lymphomatous B cells were detected within the graft cellular infiltrates, suggesting an indirect mechanism of kidney injury. Although kidney graft function partially recovered after steroid therapy, the posttransplant lymphoproliferative disorder progressed and the patient died 7 months later.
dc.format.extent4 p.
dc.format.mimetypeapplication/pdf
dc.identifier.issn2590-0595
dc.identifier.pmid21342489
dc.identifier.pmid34401733
dc.identifier.urihttps://hdl.handle.net/2445/179988
dc.language.isoeng
dc.publisherElsevier BV
dc.relation.isformatofReproducció del document publicat a: https://doi.org/10.1016/j.xkme.2021.03.011
dc.relation.ispartofKidney Medicine, 2021, vol. 3, num. 4, p. 665-668
dc.relation.urihttps://doi.org/10.1016/j.xkme.2021.03.011
dc.rightscc by-nc-nd (c) Melilli, Edoardo et al, 2021
dc.rights.accessRightsinfo:eu-repo/semantics/openAccess
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/3.0/es/*
dc.sourceArticles publicats en revistes (Institut d'lnvestigació Biomèdica de Bellvitge (IDIBELL))
dc.subject.classificationTrasplantament renal
dc.subject.classificationLeucèmia limfocítica crònica
dc.subject.otherKidney transplantation
dc.subject.otherChronic lymphocytic leukemia
dc.titleAcute Kidney Injury Following Chimeric Antigen Receptor T-Cell Therapy for B-Cell Lymphoma in a Kidney Transplant Recipient
dc.typeinfo:eu-repo/semantics/article
dc.typeinfo:eu-repo/semantics/publishedVersion

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