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Cytomegalovirus (CMV) and BK polyomavirus (BKV) infections have been described in a high percentage of renal transplant patients and are known to cause various complications in renal transplantation. They are closely related to immunosuppressive therapy and implicated in the progression of graft failure. This review focuses on the clinical aspects of CMV and BKV infection after renal transplantation, optimal monitoring, and recent preventive measures and interventions to improve graft function and recipient survival.

Polyomavirus BK (BKV) infection has been lately recognized as a major cause of renal allograft dysfunction. BKV-related interstitial nephropathy (PVAN) may affect 1-10% of renal allograft recipients, occurring more frequently in the first 6 months after transplantation. Progression to irreversible allograft failure has been observed in up to 45% of all cases; 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. PVAN pathogenesis is characterized by multiple synergizing factors, among which immunodepression plays a key role. PVAN diagnosis requires the evaluation of a renal biopsy showing polyomavirus cytopathic changes and confirming BKV through an ancillary technique such as immunohistochemistry. Given the focal nature of the disease, early diagnosis may be difficult to obtain. Thus, quantification of BKV-DNA in plasma has been suggested as surrogate marker for PVAN. To date, given the lack of controlled trials, there is no consensus on a 'standard' management of PVAN. However, evidence based on reported observations suggests that a step-wise reduction of immunosuppression, preceded by pulsed steroids in case of coexistent acute rejection, may improve outcomes. Additional options may be represented by drugs with antiviral activity, such as cidofovir, leflunomide or quinolones. Application of a preventive treatment based on viremia monitoring has been recently proposed.

Human infection by BK virus (BKV), a human papovavirus isolated from the urine of a transplanted patient, occurs early in life and is very widespread. The clinical features of the primary infection are unknown. After the primary infection, BKV remains latent in the host tissues. Immunosuppression of the host induces the activation of the latent virus; BKV has been isolated only from immunosuppressed patients so far. In our study the incidence of BKV infection in immunosuppressed children and in children with normal immunological defenses was investigated both by antibody and virus research, the cultural research of the virus being performed in the urine and other specimens, such as nasal-pharyngeal swabs and cerebrospinal fluids. Our results show that the incidence of the primary infection in immunosuppressed children is comparable to the incidence in children with normal immunological defenses. Two antigenically identical viruses, which showed only partial correlation with BKV, were isolated from the urine of two immunosuppressed children. These two viruses were considered as a same antigenic variant of the BKV prototype. Of all the subjects examined, only 9 immunosuppressed children had antibodies to the newly isolated viruses.