Polyoma BK Virus: An Oncogenic Virus?

We report a case of a 65-year-old gentleman with a history of end stage renal disease who underwent a successful cadaveric donor kidney transplant four years ago. He subsequently developed BK virus nephropathy related to chronic immunosuppressant therapy. Three years later, misfortune struck again, and he developed adenocarcinoma of the bladder. 1. Introduction BK virus is a member of the polyomavirus family. In immunocompetent individuals it is innocuous, often remaining latent in renal and urothelial cells [1]. Once immunity is compromised, such as in the renal transplant recipient, BK virus may result in graft dysfunction and even loss of the entire graft, an entity known as BK virus associated nephropathy (BKVAN) [2]. The existing literature suggests that persistently elevated levels of BK virus within transitional urothelial epithelium are associated with tumour formation and malignancy [3]. In this particular case, we attempt to highlight the potential pathologic role of BK virus in bladder cancer and in the renal transplant setting. 2. Case A 65-year-old man received a cadaveric kidney transplant after developing end stage renal disease. He had a longstanding history of hypertension and was receiving lithium therapy for many years for schizophrenia. Postoperatively, he established excellent graft function and was able to urinate normally. For long term immunosuppression, he was placed on oral prednisone, tacrolimus, and mycophenolate. In the months that followed, he continued to attend the transplant clinic on a regular basis. Six months postoperatively, he was noted to have elevated BUN and creatinine levels of 38？mg/dL and 1.86？mg/dL, respectively, from a previously normal baseline. Tacrolimus levels were checked to exclude its toxicity. A renal ultrasound was performed but was found to be negative for any leak or obstruction. BK levels were checked, and he was found to have a viral load greater than 400,000？copies/mL on two separate occasions. Doses of his immunosuppressant medications were immediately reduced. Over the next four years, he continued to undergo close surveillance with regular monitoring of serum creatinine and BK virus DNA levels. In spite of our best efforts, he eventually developed renal allograft failure. Histopathological specimens were sent. Immunohistochemical staining using the peroxidase test for SV-40 antigen was performed, and the diagnosis of renal failure secondary to BKVAN was confirmed. The patient was initiated on haemodialysis and placed on the transplant list once more. He continued to see his primary care