High Incidence of Malignancy in Polyomavirus-Associated Nephropathy in Renal Transplant Recipients

doi:10.1016/j.transproceed.2010.02.068

中山醫學大學機構典藏 CSMUIR > 醫學院 > 醫學系 > 期刊論文 > Item 310902500/11097

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Title:	High Incidence of Malignancy in Polyomavirus-Associated Nephropathy in Renal Transplant Recipients
Authors:	C.-H.Chen M.-C.Wen M.Wang J.-D.Lian C.-H.Cheng M.-J.Wu T.-M.Yu Y.-W.Chuang D.Chang K.-H.Shu
Contributors:	中山醫學大學
Date:	2010
Issue Date:	2015-07-10T04:16:18Z (UTC)
ISSN:	0041-1345
Abstract:	Human 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. Human polyomaviruses (PVs), including JC (JCV) and BK (BKV), are known to cause polyomavirus-associated nephropathy (PVAN) in 2% to 5% of renal transplant recipients in the past decade.1 BKV was first isolated in 1971 from the urine of a recipient with a ureteral stricture [2], but the incidence of PVAN did not increase until the introduction of tacrolimus and mycophenolate as immunosuppressive agents. In organ transplant patients BKV mainly invades the urinary tract and may cause hemorrhagic cystitis and PVAN. However, the prevalence of JC viruria is high in Taiwan.3 We also previously also demonstrated that JCV was able to cause PVAN.4 As a result of excessive immunosuppressive therapy, reactivation of both viruses is the main etiology of PVAN. The oncogenicity of PVs has already been documented in both animal and in vitro studies. The impact of PV (BKV and JCV) infections on neoplasms has not been established in human beings. 5, 6 and 7 In the present case series, we examined the correlation of clinical courses and malignancy among patients with PVAN.
URI:	https://ir.csmu.edu.tw:8080/ir/handle/310902500/11097 http://dx.doi.org/10.1016/j.transproceed.2010.02.068
Relation:	Transplantation Proceedings Volume 42, Issue 3, April 2010, Pages 817–818
Appears in Collections:	[醫學系] 期刊論文

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