BK viral reactivation in cardiac transplant patients: evidence for a double-hit hypothesis

BK nephropathy is a significant cause of renal dysfunction in renal allograft recipients. The question of whether BK viral infection plays a role in renal dysfunction in cardiac transplantation patients remains to be answered.

We prospectively examined the prevalence of BK viral reactivation in the setting of cardiac transplantation and performed a cross-sectional analysis of 111 cardiac transplantation patients. We also assessed the prevalence of viremia in a cohort of 29 renal transplant recipients.

We found urinary decoy cells in 28 cardiac transplantation patients. Of these, 14 patients had evidence of BK viral DNA in the urine. None, however, had evidence of BK viremia. Mean age, gender, levels of pre- and post-transplant serum creatinine, cardiopulmonary bypass time, and ischemic time were not significantly different between the groups. We found that 7 of 29 renal transplant recipients studied had BK viral DNA in their urine.

These findings are evidence of BK virus reactivation in the setting of cardiac transplantation at a percentage similar to that seen in renal allograft recipients. In contrast to renal allograft recipients, none had evidence of viremia. Thus, even in the setting of established BK virus reactivation, immunosuppression in combination with renal allograft dysfunction and renal ischemic injury is usually insufficient to cause BK viremia and nephropathy, and it appears that a second, organ-specific hit is necessary, such as kidney inflammation, kidney ischemia, or donor-recipient human leukocyte antigen mismatch.