POLYOMA VIRUS INFECTION IN THE RENAL ALLOGRAFT: A SINGLE CENTER EXPERIENCE

Abstract

136 Introduction: Polyoma virus renal allograft infection (PVI) is a known cause of renal allograft dysfunction and loss. The clinical features of 12 kidney transplant (KTX) or simultaneous kidney-pancreas transplant (SPK) recipients with PVI at a single institution were reviewed. Materials and Methods: From 12/92 to 10/98, 12 patients were diagnosed with PVI by immunoperoxidase stain and electron microscopy. We reviewed these cases analyzing preoperative characteristics, immunosuppression, disease presentation and treatment. Results: Mean patient age was 35 (range 13-66 years). Follow-up ranged from 5 to 78 months. Of the 12 transplants performed, 5 were cadaveric KTX, 3 SPK, 1 pediatric en-bloc transplant, and 3 were living related. Immunosuppression consisted of triple drug therapy in all patients. At the time of diagnosis, 67% of patients were taking tacrolimus, 33% were taking cyclosporine. Concurrently, 83% were taking mycophenolate mofetil and all patients were taking prednisone. Latency of infection ranged from 57 to 625 days with a median of 232 days. 7 patients (58%) had been treated or hospitalized for recent infections, including pneumonia (3/7), UTI (2/7), line sepsis (1/7), and CMV antigenemia (1/7). Symptoms at presentation were nonspecific and included fatigue and myalgias. Patients presented with an acute rise in creatinine ranging from 0.5 to 2.2 mg/dL (mean 1.2 mg/dL). These symptoms and findings mimicked acute rejection leading to allograft biopsy which revealed characteristic histology for polyoma. PVI was typically managed by reduction in immunosuppression. However in two patients, empiric treatment with daclizumab or steroids had been initiated prior to final tissue diagnosis. Graft loss occurred in 5 (42%) patients, and partial to full recovery of renal function occurred in 7 (58%) patients. Of those patients who suffered graft loss, two underwent re-transplant with living related kidneys. Follow-up at 6 months shows excellent graft function. Conclusion: Polyoma virus infection of the renal allograft can cause significant graft dysfunction and loss. Presentation may mimic rejection, and the diagnosis of polyoma infection should be considered on review of biopsy specimens. Decreasing immunosuppression was not completely effective in salvaging kidney function. The impact of newer immunosuppression protocols on the occurrence of polyoma, as well as the long-term outcome of re-transplantation remains to be elucidated.