Antiviral prophylaxis, male sex, and killer immunoglobulin-like receptor KIR2DL3 as markers for stratifying the risk of BK polyomavirus-associated nephropathy in kidney transplant recipients.
Journal
Polish archives of internal medicine
ISSN: 1897-9483
Titre abrégé: Pol Arch Intern Med
Pays: Poland
ID NLM: 101700960
Informations de publication
Date de publication:
24 01 2023
24 01 2023
Historique:
pubmed:
27
8
2022
medline:
26
1
2023
entrez:
26
8
2022
Statut:
ppublish
Résumé
The risk of polyomavirus‑associated nephropathy (PyVAN) currently ranges from 1% to 10%, and the risk of graft loss is 10% to 50% within 2 years post‑diagnosis. There is currently no specific antiviral therapy against BK polyomavirus (BKPyV), and no therapeutic approach has been proven superior. Natural killer cells play a key role in the defense against viral infections. A retrospective, single‑center cohort study was performed to investigate the association between the kidney transplant recipients' killer‑cell immunoglobulin‑like receptor (KIR) genotype and PyVAN. We also evaluated other possible risk factors for the occurrence of PyVAN in a population of kidney transplant recipients. DNA samples from 134 kidney transplant recipients were identified for the presence or absence of variable KIR genes and their HLA ligands using polymerase chain reaction with sequence‑specific primers. The analysis revealed that the presence of the inhibitory KIR2DL3 (P = 0.03) was a risk factor for posttransplant PyVAN. We also found that the presence of acute rejection before PyVAN (P = 0.02), male sex (P = 0.04), and the lack of antiviral prophylaxis (P = 0.01) were additional risk factors for posttransplant PyVAN. Our findings confirm that the KIR/HLA genotype plays a significant role in the development of PyVAN and suggest the contribution of both environmental and genetic factors to the incidence of BKPyV infection after kidney transplantation.
Identifiants
pubmed: 36018060
doi: 10.20452/pamw.16331
pii:
doi:
Substances chimiques
Antiviral Agents
0
KIR2DL3 protein, human
0
Receptors, KIR
0
Receptors, KIR2DL3
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM