Abstract
Epidemiology of opportunistic infections (OI) after kidney allograft transplantation in the modern era of immunosuppression and the use of OI prevention strategies are poorly described. We retrospectively analyzed a single-center cohort on kidney allograft adult recipients transplanted between January 2008 and December 2013. The control group included all kidney recipients transplanted in the same period, but with no OI. We analyzed 538 kidney transplantations (538 patients). The proportion of OI was 15% (80 and 72 patients). OI occurred 12.8 (6.0–31.2) months after transplantation. Viruses were the leading cause (n = 54, (10%)), followed by fungal (n = 15 (3%)), parasitic (n = 6 (1%)), and bacterial (n = 5 (0.9%)) infections. Independent risk factors for OI were extended criteria donor (2.53 (1.48–4.31), p = 0.0007) and BK viremia (6.38 (3.62–11.23), p < 0.0001). High blood lymphocyte count at the time of transplantation was an independent protective factor (0.60 (0.38–0.94), p = 0.026). OI was an independent risk factor for allograft loss (2.53 (1.29–4.95), p = 0.007) but not for patient survival. Post-kidney transplantation OIs were mostly viral and occurred beyond one year after transplantation. Pre-transplantation lymphopenia and extended criteria donor are independent risk factors for OI, unlike induction therapy, hence the need to adjust immunosuppressive regimens to such transplant candidates.
Highlights
Kidney allograft recipients are exposed to a broad range of infectious pathogens that give rise to infections with unusual and more severe presentations [1]
We present here the results of a monocentric cohort analysis conducted on more than 500 kidney allograft recipients
In the era of modern immunosuppression and the wide use of infectious disease prophylactic strategies, opportunistic infections (OI) occurred more than one year after transplantation and that pre-transplantation lymphopenia was an independent risk factor for OI episode, which was not the case for induction therapy
Summary
Kidney allograft recipients are exposed to a broad range of infectious pathogens that give rise to infections with unusual and more severe presentations [1]. Anti-thymocyte globulin primarily induces rapid, profound, and long-lasting depletion of T-lymphocytes in peripheral blood and lymphoid organs, and apparently it does not spare B-cell and NK cell populations [9,10]. Thanks to such therapies, patient and kidney allograft survival after kidney transplantation have markedly improved and acute allograft rejection has decreased [11,12,13].
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