BK virus in the transplant patient

Abstract

BK virus (BKV) infection after kidney transplantation has been a subject of great interest in the past decade. BKV remains latent in the urinary tract and may be reactivated in immunocompromised patients. BKV has been identified as the etiologic agent of polyomavirus-associated nephropathy (PVAN), which is a significant cause of allograft failure in renal-transplant patients. The diagnosis of PVAN requires evaluation of a renal biopsy specimen with demonstration of cytopathic changes. Patients with PVAN have demonstrated high levels of viruria and viremia. There is general agreement that BK viruria of greater than 10 7 BKV copies/ml of urine and BKV viremia of 10 4 copies of BKV/ml of plasma are typical in patients with biopsy-proven PVAN. Prospective surveillance programs of viruria and viremia can help identify those patients at risk for developing PVAN. In addition, BKV has been associated with renal dysfunction in non-renal organ transplantation. BKV viruria has been documented in a number of non-renal organ transplants with otherwise unexplained chronic renal dysfunction late in the transplant period. Additional studies to define the contribution of BKV to renal dysfunction in all transplant patients are warranted.