Urinary cytology, nucleic acid testing of urine and/or plasma, and viral-specific staining of biopsy specimens are necessary for diagnosis. Infected tubular cells show intranuclear inclusions, lysis or necrosis, and shedding into the tubular lumen. But such light microscopy findings are quite focally observed in many cases, and varying degrees of tubulointerstitial inflammation mimicking T-cell-mediated

acute rejection make accurate diagnosis difficult. There is a histological classification of BKVN originally reported by the University of Maryland in 2001, and modified by American Society of Transplantation Infectious Disease Community of Practice, which focuses on interstitial inflammation and fibrosis. Another see more classification was proposed by the Banff Working Group in 2009 (Banff Working Proposal), which focuses

on acute tubular injury instead of interstitial inflammation. The usefulness of the Banff Working Proposal is now under consideration with a multicenter study being conducted, but it has not yet reached a clear conclusion. In this review, the current screening strategies for the replication of BK virus, difficulties with diagnosis, histopathological classifications, treatments, and prognostic factors of BKVN are discussed. Polyomavirus BK (BKV) is an important pathogen in organ transplant patients. BKV was first isolated from mTOR inhibitor urine and ureteral epithelial cells of a kidney transplant patient,[1] and is known

to cause ureteral stenosis and hemorrhagic cystitis in kidney and hematopoietic stem cell transplant patients. The first case of tissue destructive nephropathy, called polyomavirus BK nephropathy (BKVN), in a kidney allograft was reported in 1995,[2] and numerous studies on various aspects of the causative virus and the disease have been published. Vasopressin Receptor BKV is ubiquitously present in the general population, and 90% or more of tested individuals may be seropositive.[3, 4] It is demonstrated that BKV is transmitted to the patient through the donor kidney with a latent infection,[5] and is reactivated with immunosuppressive treatment. Urinary shedding of the virus, called viruria, is the first step of viral reactivation, followed by viraemia, and nephropathy after the 6–12-week window period.[6] Progression of BKVN is associated with interstitial fibrosis, and subsequent acute rejection followed by the reduction of immunosuppression also induces allograft injury. Since graft survival in patients with BKVN is much poorer than those without the disease,[7] current clinical practice focuses on the early detection of viral replication and pre-emptive reduction of immunosuppression.[8-10] The management of BKV infection appeared in Kidney Disease Improving Global Outcome (KDIGO) guidelines in 2009,[8] and the American Society of Transplantation (AST) Infectious Disease Community of Practice also published guidelines.