BK viral infection after renal transplantation

Abstract

Viral infections have been a subject of great interest in patients after organ transplantations. Post-transplant immunosuppressive therapy is often associated with transfenction or reactivation of viruses. The human polyomavirus type I, also called BK virus (BKV), causes polyomavirus-associated nephropathy (PVAN) in 1-10% of renal transplant recipients. Thanks to increased PVAN awareness and improved diagnostic techniques, the rate of graft loss has lowered, more consistently in centres with active screening and intervention programs. The risk factors for PVAN are not conclusively defined and likely involve complementing determinants of recipient, graft, and virus. Central element seems to be the failing balance between BKV replication and BKV-specific immune control, which can result from intense triple immunosuppression, HLA-mismatches, prior rejection and anti-rejection treatment, or BKV-seropositive donor/seronegative recipient pairs. PVAN diagnosis requires the evaluation of a renal biopsy showing polyomavirus cytopathic changes and confirming BKV through an ancillary technique such as immunohistochemistry. The success rate of the intervention is increased with earlier diagnosis. Therefore, it is recommended that all renal transplant recipients should be screened for BKV replication in urine and serum. The treatment of BKVN consists mainly of reduction in immunosuppressive therapy. Currently, in the clinical management of PVAN, no satisfactory antiviral treatment has been defined. Retransplantation after renal allograft loss to PVAN remains a treatment option for patients clearing polyomavirus replication.