MEI-LIN WANG2026-10-162026-10-162010-01-01Pure ID: 15072763Pure UUID: 118ac924-06b5-4d35-9410-8601db56cebe10.1016/j.transproceed.2010.02.068https://www.scopus.com/pages/publications/77955487113https://scholars.csmu.edu.tw/handle/123456789/25357Human polyomaviruses (PV), including JC and BK virus, have been reported to cause polyomavirus-associated nephropathy (PVAN), in renal transplant patients. PV infection has been demonstrated to be associated with malignancies in animals; however, the association between malignancy and viral infections in humans is not clear. We retrospectively reviewed our 864 (M:F = 502:362) kidney transplant patients over the past 25 years. We identified PVAN in 6 patients (0.69%), including BK nephropathy (n = 5) and JC nephropathy (n = 1). Three patients (50%) improved after reducing the immunosuppression, but 3 (50%) progressed to graft loss despite this reduction. Malignancy occurred in 5 out of the 6 patients (83%; P <.0001 compared with patients without PVAN), including transitional cell carcinoma (n = 2), renal cell carcinoma (n = 1), squamous cell carcinoma of skin (n = 1) and Kaposi sarcoma (n = 1). We concluded that kidney transplant patients with PVAN are at a significantly greater risk to develop malignancy. Whether this is due to a direct effect of PV infection or the result of overimmunosuppression remains to be determined in a future study.2enjournal article