Risk factors for BK nephropathy in kidney or simultaneous kidney=pancreas allograft recipients

Background. Until recently, BK polyomavirus (BKV) nephropathy was misdiagnosed and mistreated as steroid-resistant acute rejection. In such cases the infection was spreading, which inevitably led to graft failure. Now it is known that the only way to control the disease is to decrease the net state of immunosuppression. Objectives. Assessment of incidence of BKV nephropathy. Material and Methods. One hundred twelve patients qualified for kidney or pancreas-kidney transplantation were included in the study. Before transplantation and after 1, 3, 6, 12, and 24 months, blood samples were collected for real-time PCR tests in all patients. Renal biopsies were performed in case of creatinine level increase, after the exclusion of extrarenal causes. All specimens were stained (by immunohistochernistry) for the presence of the large T antigen of SV40 virus (similar to the large T antigen of BKV). Clinical data on the kind of transplantation, total ischemia time, immunosuppressive treatment, postoperative oliguria, acute rejection episodes and their treatment with steroid boluses, and creatinine level were acquired. Results. Viremia incidence in the study group was 27.96% (after six months: 18%, after 12 months: 25.5%, after 24 months: 27.96%) and the BK nephropathy incidence was 7.85% (3 cases). Increased risk of the viremia was observed in cases of retransplantation (RR = 4.93, p < 0.001), acute rejection treatment with steroid boluses (RR = 3.13, p < 0.008), coexisting viral infections with hepatitis B virus (RR = 9.3, p < 0.003), herpes simplex virus (RR = 3.08, p < 0.024) and varicella-zoster virus (RR = 2.76, p = ns), and total ischernia time longer than 25 hours (RR = 2.62, p < 0.048). The kind of immunosuppressive drugs, their blood concentrations, induction treatment with antibody preparations, simultaneous kidney and pancreas transplantation (versus kidney alone transplantation), cytomegalovirus and hepatitis C infections, and diabetes or urinary tract infection had no significant influence on the incidence of viral replication. Viral load was over 5000 copies/ tl in these cases. Conclusions. It can be stated that the incidence of BKV infection and its natural history are similar to those described in other transplantation centers in the world. Factors leading to tubular epithelial cell damage and other viral infections are risk factors for BKV replication (Adv Clin Exp Med 2008, 17, 2, 201-206).