No Major Effect of Innate Immune Genetics on Acute Kidney Rejection in the First 2 Weeks Post-Transplantation.

IL6 -6331 acute rejection immune genetics kidney transplantation tacrolimus

Journal

Frontiers in pharmacology
ISSN: 1663-9812
Titre abrégé: Front Pharmacol
Pays: Switzerland
ID NLM: 101548923

Informations de publication

Date de publication:
2019
Historique:
received: 14 10 2019
accepted: 24 12 2019
entrez: 11 3 2020
pubmed: 11 3 2020
medline: 11 3 2020
Statut: epublish

Résumé

Innate immunity contributes to acute rejection after kidney transplantation. Genetic polymorphisms affecting innate immunity may therefore influence patients' risk of rejection. To investigate the effect of recipient and donor This study included 154 kidney transplant recipients and 81 donors successfully genotyped for 17 polymorphisms in these genes. All recipients were under triple immunosuppressant therapy of TAC, mycophenolate mofetil, and prednisolone. Recipient and donor genotype differences in acute rejection incidence within the first 2 weeks post-transplantation were assessed by logistic regression, adjusting for induction therapy, human leukocyte antigen mismatches, kidney transplant number, living donor, and peak panel-reactive antibody scores. A trend (Cochran-Armitage P = 0.031) of increasing acute rejection incidence was observed from recipient This study did not detect any statistically significant effects of recipient or donor innate immune genetics on acute rejection incidence in the first 2 weeks post-transplantation. However, the sample size was small, and future larger studies or meta-analyses are required to demonstrate conclusively if innate immune genetics such as

Sections du résumé

BACKGROUND BACKGROUND
Innate immunity contributes to acute rejection after kidney transplantation. Genetic polymorphisms affecting innate immunity may therefore influence patients' risk of rejection.
OBJECTIVE OBJECTIVE
To investigate the effect of recipient and donor
METHODS METHODS
This study included 154 kidney transplant recipients and 81 donors successfully genotyped for 17 polymorphisms in these genes. All recipients were under triple immunosuppressant therapy of TAC, mycophenolate mofetil, and prednisolone. Recipient and donor genotype differences in acute rejection incidence within the first 2 weeks post-transplantation were assessed by logistic regression, adjusting for induction therapy, human leukocyte antigen mismatches, kidney transplant number, living donor, and peak panel-reactive antibody scores.
RESULTS RESULTS
A trend (Cochran-Armitage P = 0.031) of increasing acute rejection incidence was observed from recipient
CONCLUSIONS CONCLUSIONS
This study did not detect any statistically significant effects of recipient or donor innate immune genetics on acute rejection incidence in the first 2 weeks post-transplantation. However, the sample size was small, and future larger studies or meta-analyses are required to demonstrate conclusively if innate immune genetics such as

Identifiants

pubmed: 32153387
doi: 10.3389/fphar.2019.01686
pmc: PMC7045476
doi:

Types de publication

Journal Article

Langues

eng

Pagination

1686

Informations de copyright

Copyright © 2020 Hu, Barratt, Coller, Sallustio and Somogyi.

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Auteurs

Rong Hu (R)

Discipline of Pharmacology, Adelaide Medical School, University of Adelaide, Adelaide, SA, Australia.

Daniel T Barratt (DT)

Discipline of Pharmacology, Adelaide Medical School, University of Adelaide, Adelaide, SA, Australia.

Janet K Coller (JK)

Discipline of Pharmacology, Adelaide Medical School, University of Adelaide, Adelaide, SA, Australia.

Benedetta C Sallustio (BC)

Discipline of Pharmacology, Adelaide Medical School, University of Adelaide, Adelaide, SA, Australia.
Department of Clinical Pharmacology, The Queen Elizabeth Hospital, Adelaide, SA, Australia.

Andrew A Somogyi (AA)

Discipline of Pharmacology, Adelaide Medical School, University of Adelaide, Adelaide, SA, Australia.
Department of Clinical Pharmacology, Royal Adelaide Hospital, Adelaide, SA, Australia.

Classifications MeSH