%0 Journal Article
%T Ureteral Stent Placement Increases the Risk for Developing BK Viremia after Kidney Transplantation
%A Faris Hashim
%A Shehzad Rehman
%A Jon A. Gregg
%A Vikas R. Dharnidharka
%J Journal of Transplantation
%D 2014
%I Hindawi Publishing Corporation
%R 10.1155/2014/459747
%X The placement of ureteral stent (UrSt) at kidney transplantation reduces major urological complications but increases the risk for developing nephropathy from the BK virus. It is unclear whether UrSt placement increases nephropathy risk by increasing risk of precursor viral replication or by other mechanisms. We retrospectively investigated whether UrSt placement increased the risk for developing BK Viremia (BKVM) in adult and pediatric kidney transplants performed at the University of Florida between July 1, 2007, and December 31, 2010. In this period all recipients underwent prospective BKV PCR monitoring and were maintained on similar immunosuppression. Stent placement or not was based on surgeon preference. In 621 transplants, UrSt were placed in 295 (47.5%). BKVM was seen in 22% versus 16% without UrSt ( ). In multivariate analyses, adjusting for multiple transplant covariates, only UrSt placement remained significantly associated with BKVM ( ). UrSt placement significantly increased the risk for BKVM. Routine UrSt placement needs to be revaluated, since benefits may be negated by the need for more BK PCR testing and potential for graft survival-affecting nephritis. 1. Introduction BK virus (BKV) was first isolated in 1971 from the urine of a Sudanese renal transplant recipient who presented with ureteral stenosis [1]. Years later, a new era in the study of BKV began when BK nephropathy (BKN) was diagnosed by a needle biopsy in a renal transplant (RTx) recipient suspected of having acute rejection [2]. In the following years, additional cases were reported from kidney transplant centers worldwide [3¨C5]. In nonimmunosuppressed hosts, BKV infection remains latent and asymptomatic in uroepithelial cells, though a fraction of asymptomatic seropositive subjects shed virus into the urine [6]. In states of immunosuppression, such as after kidney transplantation, BKV is reactivated and infection can progress from viruria to viremia, followed by nephropathy [7]. Efforts to eradicate this problem have included the identification of risk factors, early detection of BK viruria (BKVU) and BK viremia (BKVM) through serial PCR screening, early diagnostic biopsy for allograft dysfunction, minimization of immunosuppression for biopsy-proven BKN, and the employment of pharmacotherapy [8]. Risk factors for BKV infection include a higher degree of human leukocyte antigen mismatch, pediatric status, aggressive immunosuppressive regimen, and transplant ureteral stent use [9]. The role of stents is controversial. In two prior single center adult studies, the placement of
%U http://www.hindawi.com/journals/jtrans/2014/459747/