**Abstract**

Opportunistic infections commonly occur during the first 6 months after kidney transplant, including cytomegalovirus (CMV) and polyomaviruses. Viral pathogens such as CMV and polyomaviruses, JC or BK virus (BKV), are able to replicate in the kidney and/or cause systemic disease, and symptomatic infection with these agents can be associated with significant morbidity and mortality in immunocompromised host. While BK virus usually replicates in kidney transplant causing BK virus nephropathy (BKN) with characteristic decoy cells in the urine, CMV infection more often leads to systemic infection involving the gastrointestinal tract (GIT), lungs, or liver and can only sporadically be detected in renal transplant. In both cases, the disease is most often due to reactivation of a latent virus. Prevention and early treatment of posttransplant infection are therefore crucial with kidney transplant recipients. Since BKV viruria and viremia can be seen without renal injury and viral nephropathy, a diagnosis of BKN must be confirmed by renal biopsy. To date, preemptive treatment is the best strategy for CMV infection, while no available standard therapy, except for reduction of immunosuppression, is available for BKV infection.

**Keywords:** CMV, BK, cytomegalovirus, polyomavirus, viral infections, kidney transplantation

### **1. Introduction**

CMV and polyomavirus infection is common in the human population and mainly remains asymptomatic through the life of healthy individuals. However, in immunocompromised individuals, such as kidney transplant recipients (KTRs), it can be associated with various complications, including direct systemic effects of viral infection, bacterial or fungal superinfection, viral infection of the transplanted kidney, and acute and chronic rejection, which consequently diminish patient and graft survival. Current preventive strategies in KTRs include preemptive therapy with valganciclovir or intravenous ganciclovir and universal prophylaxis with antivirals after kidney transplantation and for 1–3 months after treatment with antilymphocyte antibodies. Strategies to control established virus infection include decreasing immunosuppression, adding antivirals, and a combination of both [1–3].

BK virus nephropathy is the most common manifestation of BKV reactivation after renal transplantation, leading to loss of renal grafts in approximately 43% of patients. BKV viruria and viremia can be seen without renal injury and viral nephropathy, so renal biopsy remains the gold standard for definite BKN diagnosis. Therapeutic strategies of BKN management are still very limited, so screening

protocols in order to detect early BK reactivation are important. BKN might be successfully managed with a reduction of baseline immunosuppression but is potentially harmful since it may be associated with increased risk of rejection [4–6].
