Literature DB >> 31677358

Pseudomonas aeruginosa and acute rejection independently increase the risk of donor-specific antibodies after lung transplantation.

Hrishikesh S Kulkarni1, Kevin Tsui2, Suraj Sunder1, Alex Ganninger1, Laneshia K Tague1, Chad A Witt1, Derek E Byers1, Elbert P Trulock1, Ruben Nava3, Varun Puri3, Daniel Kreisel3, Thalachallour Mohanakumar4, Andrew E Gelman3,5, Ramsey R Hachem1.   

Abstract

Factors contributing to donor-specific HLA antibody (DSA) development after lung transplantation have not been systematically evaluated. We hypothesized that the isolation of Pseudomonas aeruginosa in respiratory specimens would increase the risk of DSA development. Our objective was to determine the risk of DSA development associated with the isolation of Pseudomonas aeruginosa after lung transplantation. We conducted a single-center retrospective cohort study of primary lung transplant recipients and examined risk factors for DSA development using Cox regression models. Of 460 recipients, 205 (45%) developed DSA; the majority developed Class II DSA (n = 175, 85%), and 145 of 205 (71%) developed DSA to HLA-DQ alleles. Univariate time-dependent analyses revealed that isolation of Pseudomonas from respiratory specimens, acute cellular rejection, and lymphocytic bronchiolitis are associated with an increased risk of DSA development. In multivariable analyses, Pseudomonas isolation, acute cellular rejection, and lymphocytic bronchiolitis remained independent risk factors for DSA development. Additionally, there was a direct association between the number of positive Pseudomonas cultures and the risk of DSA development. Our findings suggest that pro-inflammatory events including acute cellular rejection, lymphocytic bronchiolitis, and Pseudomonas isolation after transplantation are associated with an increased risk of DSA development.
© 2019 The American Society of Transplantation and the American Society of Transplant Surgeons.

Entities:  

Keywords:  alloantibody; antibody biology; clinical research/practice; graft survival; immunobiology; infection and infectious agents - bacterial; lung (allograft) function/dysfunction; lung transplantation/pulmonology

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Substances:

Year:  2019        PMID: 31677358      PMCID: PMC7103544          DOI: 10.1111/ajt.15687

Source DB:  PubMed          Journal:  Am J Transplant        ISSN: 1600-6135            Impact factor:   8.086


  50 in total

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Review 9.  Lung transplant infection.

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