Abstract
Context: BK virus (BKV) viremia and BKV-associated nephropathy (BKVAN) have become a serious nuisance to kidney transplant (KT) patients since the mid-nineties, when the incidence of this disease has increased significantly. Evidence Acquisition: Directory of open access journals (DOAJ), EMBASE, Google Scholar, PubMed, EBSCO, and Web of Science have been searched. Results: Many hypothesis have been made as to why this phenomenon has developed; it is of general opinion that a more potent immunosuppression is at the core of the problem. The use of the association of tacrolimus (TAC) with mycophenolic acid (MPA) has gained momentum in the same years as the increase in BKV viremia incidence making it seem to be the most likely culprit. m-TOR inhibitors (m-TORIs) have been shown to have antiviral properties in vitro and this fact has encouraged different transplant teams to use these agents when confronted with BKV infection (viremia or nephropathy). However, the results are mitigated. There had been conflicting results for example when converting from TAC-to sirolimus-based immunosuppression in the setting of established BKVAN. Conclusions: In order to prevent BKV infection we have to minimize to some extent immunosuppression, but it is not always possible, e.g. in high immunological risk patients. Conversely, we could use m-TORIs associated with low-dose calcineurin inhibitors (CNIs). This could be actually the key to a safe immunosuppression regimen both from the immunological stand point and from the viral one.
Highlights
Context: BK virus (BKV) viremia and BKV-associated nephropathy (BKVAN) have become a serious nuisance to kidney transplant (KT) patients since the mid-nineties, when the incidence of this disease has increased significantly
Risk factors for having a treatment for BKV infection include the use of antithymocyte globulins as part of the induction scheme, receiving tacrolimus (TAC)based immunosuppression instead of cyclosporine A (CsA)-based immunosuppression, having MMFcontaining regimen instead of no anti-metabolitecontaining regimen, and steroid therapy; sirolimus (SRL)-based immunosuppression as opposed to CsA-based immunosuppression had a protective effect [7]
Cidofovir treatment has been attempted; its nephrotoxicity limits its clinical use [11]. Another strategy would be to modify immunosuppression when BKV infection occurs by eliminating mycophenolic acid (MPA) and replacing it by m-TOR inhibitors and decreasing calcineurin inhibitor therapy or converting from TAC to CsA
Summary
Context: BK virus (BKV) viremia and BKV-associated nephropathy (BKVAN) have become a serious nuisance to kidney transplant (KT) patients since the mid-nineties, when the incidence of this disease has increased significantly. 3. Results In the setting of organ transplant patients, BKV infection occurs mainly in kidney transplant (KT) patients; in that group of patients the prevalence of viruria, viremia and BKV-associated nephropathy (BKVAN) is as high as 30%, 13%, and 8% respectively [4].
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