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Kidney transplantation is a well-established therapy for end-stage kidney disease and provides very good long-term kidney-allograft survival provided there is adequate immunosuppression. However, transplantation [4]. This BKV replication has a major negative impact on the kidney allograft, i.e., it induces BKV-associated nephropathy every attempt to minimize immunosuppression substantially has been disastrous and has resulted in acute rejection episodes and/or the de novo occurrence of donor-specific alloantibodies, causing antibodymediated rejection [1]. Conventional immunosuppression includes a first phase where patients receive an induction therapy (lymphocyte-depleting agents or basiliximab therapy) in addition to, in most cases, high doses of a calcineurin inhibitor (CNI: cyclosporine A or tacrolimus), plus an antimetabolite (mycophenolic acid [MPA] or azathioprine), and high doses of steroids. At three to six months post-transplantation, lower doses of CNI are needed (plus an antimetabolite), with or without very low doses of steroids. Chronic immunosuppression has many drawbacks such as opportunistic infections over the short term, mostly viral infections (i.e., cytomegalovirus [CMV], BK virus [BKV] infections), and de novo cancers in the longer term, which are mostly driven by viruses such as Epstein-Barr virus (EBV), human papilloma virus (HPV), and human herpes 8 (HHV8). Until two decades ago, themajor concernwasCMV-associated infection or disease that caused direct and indirect effects such as decreased patient and graft survival, post-transplant de novo diabetes, cardiovascular morbidity, etc. [2]. However, when efficacious anti-CMV agents became available, i.e., ganciclovir and valganciclovir, the burden of CMV infection was decreased significantly. Nonetheless, the cost of anti-CMV agents is very high, and in countries where it is not reimbursed (e.g., Brazil), the incidence of CMV infection/disease within the first year post-transplantation can be as high as 37.6% in kidneytransplant patients that have had no CMV prophylaxis and where immunosuppression has relied on tacrolimus + MPA+ steroids [3]. Because CMV infection became of lesser concern,we havewitnessed an increase in BKV infection (e.g., BKV viruria and BKV viremia), which

ebiomedicine

Negative Impact of CMV and BKV Infections on Kidney-Allograft Function at 1-Year Post-Transplantation: Can it Be Changed by Modifying Immunosuppression?