• Pol. Arch. Med. Wewn. · Jan 2023

    Antiviral prophylaxis, male gender and killer immunoglobulin-like receptor KIR2DL3 as markers for stratifying the risk of BK polyomavirus-associated nephropathy in kidney transplant recipients.

    • Dominika Dęborska-Materkowska, Agnieszka Perkowska-Ptasinska, Anna Sadowska-Jakubowicz, Joanna Pazik, Marta Serwańska-Świętek, Natalia Mikołajczyk, Robert Świder, Jacek Nowak, and Magdalena Durlik.
    • Department of Transplantation Medicine, Nephrology and Internal Diseases, Medical University of Warsaw, Warsaw, Poland. dominika.deborska-materkowska@wum.edu.pl
    • Pol. Arch. Med. Wewn. 2023 Jan 24; 133 (1).

    IntroductionThe 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.ObjectivesA 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.Patients And MethodsDNA 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.ResultsThe 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.ConclusionsOur 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.

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