Update on pathological features of polyomavirus allograft nephropathy

PURPOSE OF REVIEW: The availability of potent immunosuppressant drugs has resulted in an increasing incidence of viral infections in solid organ transplantation. Of particular interest is the occurrence of polyomavirus allograft nephropathy. This affects 5-10% of kidney transplant recipients and is associated with a high risk of premature graft loss. RECENT FINDINGS: Histologically proven polyomavirus allograft nephropathy is preceded by a period of asymptomatic viruria and the eventual development of viremia. Systematic determinations of viruria and viremia have demonstrated that although polyomavirus infections are quite common in the first months following transplantation, only a minority of patients develop full blown polyomavirus allograft nephropathy. Progression of the condition leads to end-stage renal disease characterized by tubular atrophy, interstitial fibrosis and chronic inflammation. Early on, renal involvement is focal and liable to tissue sampling errors (false negative biopsy). Interpretation of the renal biopsy in the context of the viral loads (viruria, viremia), however, allows for early diagnosis even if the biopsy fails to demonstrate the viral cytopathic changes. SUMMARY: Recognition of the sequence of events leading to polyomavirus allograft nephropathy (viruria-viremia-nephritis) has provided the rational basis for screening protocols to identify patients at risk. Reduction of immunosuppression before irreversible renal scarring develops has resulted in a marked decrease in graft loss due to polyomavirus allograft nephropathy.