Abstract
BK virus (BKV) may cause nephropathy in renal transplant recipients receiving immunosuppressive therapy, resulting in renal dysfunction and, possibly graft loss. However, the positive and negative predictive values of BK viral load are still controversial. In this prospective, single-center study, BKV DNA was measured 1, 3 and 6 months after transplantation. The viral load in urine and plasma was quantified with the real-time Q-PCR (Argen kit) in 73 renal allograft recipients Three of them showed acute rejection. To determine the cutoff value of viral load, 60 sera samples of healthy blood donors, matched for age and sex, were tested. The mean plasmatic viral load one month posttransplantation was statistically higher in renal transplant recipients (17.23 copies/ml) compared to that in controls (2 copies/ml) (p: 0.06). This difference of the distribution of viremia values is more evident in the third and sixth month (p: 0.002 and 0.010 respectively). Furthermore, analysis of the kinetic of viral load revealed an average rise of viremia at 3 months (1589.14 copies/ml) followed by its decrease at 6 months (249.75 copies/ml). However, the difference was not statistically significant. The same is true for the distribution of values of viruria and in all cases the average viral load was statistically higher in urine than in plasma. In addition, this study did not shown significant relationsheep between viremia/viruria and the occurrence of acute rejection, the renal function deterioration, the source of allograft or immunosuppressive therapy protocol. If the results of this study demonstrate the importance of the replication of BKV in renal transplant patients from the first month compared to that in immunocompetent subjects, the screening of the DNA of this virus does not appear to have a prognostic value in the occurrence of acute rejection. However, the plasma and urine monitoring of BKV load beyond 6 months, not appear to exclude the relationsheep between these two biomarkers and the occurrence of chronic graft dysfunction.
Highlights
BK virus (BKV) is a non-enveloped DNA virus, belonging to the Polyomaviridae family
The viral load in urine and plasma was quantified with the real-time quantification by real-time PCR (Q-PCR) (Argen kit) in 73 renal allograft recipients Three of them showed acute rejection
If the results of this study demonstrate the importance of the replication of BKV in renal transplant patients from the first month compared to that in immunocompetent subjects, the screening of the DNA of this virus does not appear to have a prognostic value in the occurrence of acute rejection
Summary
BK virus (BKV) is a non-enveloped DNA virus, belonging to the Polyomaviridae family. It is ubiquitous with specific host spectra. BKV reactivation in urinary tractus, which is usually asymptomatic viruria, may occur in both immunocompetent subjects, and immunocompromised patients leading to polyomavirus associated nephropathy (PVAN) that has recently reported as a cause of allograft failure in renal transplant recipients. This nephropathy seems to be related to the conjunction of an intensive immunosuppressive regiments containing tacrolimus (Tac) or mycophenolate mofetil (MMF), an immuno-allogenic environment, a viral reactivation and a renal tubular damages caused by ischaemia or rejection [1,2,3,4]. Diagnosis of PVAN is based on the presence of cells with intranuclear viral inclusions, known as “decoy cells” and the histological inconstant viral alterations in specimens from allograft biopsies [2,8] or research of large T viral antigen by a standard immunohistochemical staining
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
