BK VIRUS INFECTION

J.L. Descourouez¹, D.R. Hager², B.J. Voss³, G.E. Leverson³, B.N. Becker⁴, R.M. Hofmann⁴, A. Djamali⁵, J. Pirsch^6
1Department Of Pharmacy, University of Wisconsin Hospital and Clinics, Madison/UNITED STATES OF AMERICA, ²Department Of Pharmacy, University of Wisconsin Hospital and Clinics, Madison/WI/UNITED STATES OF AMERICA, ³Department Of Surgery, University of Wisconsin School of Medicine and Public Health, Madison/WI/UNITED STATES OF AMERICA, ⁴Medicine, University of Wisconsin School of Medicine and Public Health, Madison/WI/UNITED STATES OF AMERICA, ⁵Medicine And Surgery, University of Wisconsin, Madison/WI/UNITED STATES OF AMERICA, ⁶Medicine And Surgery, University of Wisconsin, Madison/UNITED STATES OF AMERICA

Body: Background: BK virus has become one of the leading pathogens implicated in graft loss and dysfunction following kidney transplant. Recently, the incidence of BK nephropathy has increased, prompting multiple studies which have explored possible risk factors for the development of BK virus infection. However, a variety of induction immunosuppressive therapies have yet to be investigated. In particular, alemtuzumab has not been assessed as a risk factor for development of BK viruria and viremia. We examined potential risk factors for the activation or reactivation of BK virus following kidney, simultaneous kidney-pancreas (SPK), and pancreas after kidney (PAK) transplant using a retrospective databank analysis. During this time, a variety of induction protocols were used allowing us to examine the effect of induction agent on the incidence of BK viral activation. Additionally, we determined the incidence of BK viruria/viremia at one-year post transplant. Methods: Between January 2003 and December 2007 a total of 1608 adult transplants (806 deceased-donor kidney, 541 living-donor kidney, 220 simultaneous kidney-pancreas (SPK), and 41 pancreas after kidney (PAK)) that survived at least one year post-transplant were performed at our institution. Of these, 33.5% (n = 538) went on to develop BK viruria/viremia. BK viruria/viremia was defined as either positive BK urine cytology, BK plasma PCR or BK virus nephropathy on biopsy. Donor and recipient risk factors for these patients were evaluated for their association with the development of BK viruria/viremia using Kaplan-Meier analyses and Cox-Proportional Hazards models. Results: At 1-year post-transplant, the rate of BK viruria/viremia by transplant type was as follows: 30.6% deceased-donor kidney, 32.3% SPK, 30.1% living-donor kidney, and 26.8% PAK. In the deceased-donor kidney group, being discharged on a calcineurin inhibitor as maintenance therapy significantly increased the risk of developing BK viruria/viremia (cyclosporine p=0.0366 and tacrolimus p=0.0026). Maintenance immunosuppression was not found to be significant in the other transplant types. Alemtuzumab was the most commonly used induction agent (53.5%, n=860), followed by basiliximab (35.0%, n=563), antithymocyte globulin (rabbit) (5.97%, n=96), none (5.39%, n=85), antithymocyte globulin (equine) (0.19%, n=3), and daclizumab (0.06%, n=1). There was no difference in the incidence of BK viruria/viremia between subjects receiving alemtuzumab for induction and those receiving other or no induction agents. None of the following donor demographics were found to be significant in any transplant type: age, race, sex, and use of an expanded criteria donor organ. Amongst recipient demographics, none of the following were found to be significant in any transplant type: age, sex, race, presence of delayed graft function, acute rejection at 30 days and diabetes. Conclusion: In our center, no pre-transplant risk factors were identified which significantly increase the risk of development of BK viruria/viremia following kidney transplant, underscoring the need for universal screening for BK viruria/viremia following kidney transplant. Maintenance immunosuppression with a calcineurin inhibitor increases the risk for development of BK viruria/viremia following deceased-donor kidney transplant, while choice of induction agent does not result in a significant increase in the incidence of BK viruria/viremia in any transplant type.

Disclosure: All authors have declared no conflicts of interest.