BK VIRUS INFECTION

F. Tinti¹, A.P. Mitterhofer², V. Pietropaolo³, M. Barile¹, D. Fioriti³, M. Mischitelli³, A. Limonta⁴, A. Meçule¹, G. Ferretti⁵, L. Poli⁵, F. Chiarini³, P. Berloco⁵, G. Taliani^4
1Nephrology, Sapienza University of Rome, Rome/ITALY, ²Clinical Medicine, Sapienza Università di Roma, Rome/ITALY, ³, Sapienza University of Rome, Rome/ITALY, ⁴Infectious And Tropical Diseases, Sapienza University of Rome, Rome/ITALY, ⁵Surgery And Transplant Organs, Sapienza University of Rome, Rome/ITALY

Body: INTRODUCTION Polyomavirus BK (BKV) infection is ubiquitous in the human population and occurs during early childhood. This infection remains asymptomatic in immunocompetent individuals. BKV viremia is considered a marker of infection and is undetectable in plasma of healthy subjects. Immunosuppression is considered the primary risk factor for the onset of BKV replication but many different factors such as local injury/regeneration, recipeint’s conditions, donor’s characteristics or graft features would promote BKV replication. In addition, PVAN seems to have a predilection for transplant kidney as compared to native kidney of patients with other transplants and the reason of this phenomenon has not been clarified. Patients on renal replacement therapy are considered an immunocompromised population, but the BKV plasma replication has never been evaluated before in these patients. Aim of our study was to investigate the prevalence of plasma and urine BKV viral load in renal transplant patients before and 3 months after transplantation; to evaluate the association of BKV infection with recipients, donors and grafts features. METHODS Since 2006 to 2008, 60 patients on dialysis listed for renal transplant in our centre (38 M/22 F) who underwent to cadaveric kidney transplantation were enrolled (T-Group). BKV load was measured by qualititative polymerase chain reaction (Ql-PCR) on plasma (60 samples) and urine (4 samples) before transplant. BKV load was measured by quantitative real-time polymerase chain reaction (Qt-PCR) post-transplant (T0) and 3 months (T3) thereafter on plasma and urine. Urea, creatinine, blood count, serum sodium and potassium were also monitored. Clinical data of patients (age and gender, etiology of end stage renal disease, presence of HCV, HBV and CMV infection, diabetes, months of renal replacement therapy, re-transplantation) were recorded; donors data (age, gender, weight, BMI and cause of death) and grafts characteristics (score and cold ischemia time) were recorded. In all patients immunosuppression included basiliximab as induction therapy, tacrolimus or cyclosporine associated with mycophenolate mofetil and steroids as maintenance therapy. RESULTS Pre transplant Ql-PCR on plasma resulted positive in 12 patients (20%), Ql-PCR on urine resulted positive in all 4 patients with diuresis. The occurrence of viremia at T0 was 33%, at T3 was 38%. Of these positive patients 11 out of 20 (55%) at T0 and 10 out of 16 (62%) at T3 were already pre-transplant viremic. Twelve pre-tranplant positive patients remain positive at T0 and 11 at T3 (1 patient lost at follow-up). Moreover 21 (35%) patients at T0 and 11 (26%) at T3 turned positive in plasma and/or urine. We did not find any association between pre-transplant viral replication and patients characteristics. Moreover we did not find any association between BKV plasma and/or urine replication or number of copies and recipient characteristics, donors parameters or graft features. CONCLUSION We evidenced for the first time, that patients on dialysis are an infected population with plasma active BKV replication, maybe cause of their immunodepression condition. In our study, this condition seems to be the principal risk factor of BKV replication in renal transplant patients in the first 3 months post-transplant.

Disclosure: All authors have declared no conflicts of interest.