BK virus reactivation and disease is emerging as an important cause of allograft dysfunction and loss, and the incidence of BK virus reactivation and disease appears to be rising. This has been attributed to the recent use of newer, highly potent immunosuppressive agents. Little is known about the biologic behavior of the virus after reactivation and its progression to disease. Also, no accepted approach to deal with the issue of BKV exists. The authors present results of an interim analysis of their ongoing prospective, randomized controlled trial of renal transplant recipients randomized to receive either tacrolimus or cyclosporine, to determine the incidence of BK virus reactivation and disease, as well as the preliminary results of a management strategy centered around preemptive reduction of immunosuppression upon detection of BK viremia in an attempt to prevent BK nephropathy. Their findings suggest that it is the overall intensity of immunosuppression, and not individual agents, that determines BKV reactivation. Active surveillance is useful because on detection of viremia, preemptive reduction of immunosuppression has led to clearance of viremia in almost 90% of cases with no progression to disease thus far.
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