Infected Donor Organs as the Main Source for BK Viremia in Kidney Recipients?

Abstract

Introduction: BK-virus (BKV) infection may lead to polyomavirus BK-associated nephropathy (PVAN), which is a serious complication after renal transplantation (RTX) and may lead to allograft loss. The exact etiology is still unknown. Concerning BK-seropositivity of more than 90% in general population PVAN could either be caused by a new infection or reactivation of the virus from the recipient or by augmented replication of the persistent virus in the allograft. Aim of this retrospective single-center analysis was to detect the prevalence of BK viremia of kidney transplant recipients and search the main infection source of polymaviruses in transplanted kidneys. Methods: BKV-screening was made by serum-PCR in 506 patients (pts) who were transplanted during January 2005 and June 2011. Furthermore we examined the BK viremia of the recipients who received the “partner kidney” from the same donor of the BKV positive patients and compared them with recipients from the “partner kidney” of a negative group. Results: From 506 kidney transplant recipients with at least one assessment of BK-PCR, PCR became positive (VL > 500 cop/ml) in exactly 100 pts (19.8%). In 33 cases from these pts the contralateral kidney was also transplanted in our centre and the BK viremia of these recipients could be followed up. In 18 (54.6%) recipients of the contralateral kidney (“partner recipient”) BK viremia could also be detected. In 10 (30.3%) “partner recipients” the BKV-PCR was negative and in 5 (15.2%) cases no BKV-PCR was made. In a coincidentally chosen BKV negative group of 100 pts, in 27 cases the contralateral kidney was transplanted in our centre and therefore could be followed up. In only 1 (3.7%) case positive BK viremia could be found. In 18 (66.7%) BKV-PCR was negative and in 8 (29.6%) cases no BKV-PCR was made. Conclusion: The prevalence of BK viremia in kidney transplanted patients in our centre is high (19.8%). In 54.6% of the BKV positive cases, where the contralateral kidney was also transplanted in our centre, the recipient of the “partner recipients” also developed a BK viremia compared to only 3.7% BKV positive cases in recipients of the contralateral kidney from our BKV negative patients. This indicates that infected donor organs could be mainly responsible for BK viremia and therefore for PVAN. Multi-centre studies with more data are necessary to confirm this assumption.