Introduction. Cytomegalovirus (CMV) and polyoma virus BK (BKV) may both establish
latency following primary infection. Frequent reactivation of these viruses can occur in the
kidney transplant recipients. BKV may induce CMV gene expression by stimulating
cellular regulator proteins or by its own gene regulator proteins. A high rate of concurrent
CMV infections has been noted in kidney transplant recipients with polyoma virus-
associated nephropathy (PVAN).
Methods. PVAN was identiﬁed in 10 of 191 patients who received kidney transplants
between October 1998 and September 2003. PVAN was conﬁrmed by allograft kidney
biopsy. Four of the 10 patients were complicated by concurrent CMV infection.
Results. Two patients had only serological evidence of CMV infection and one patient
had CMV gastritis. These three patients were treated with intravenous ganciclovir with
good results. Disseminated ganciclovir-resistant CMV disease was demonstrated in the
remaining patient. This 34-year-old kidney transplant recipient with PVAN died of
multiorgan failure despite antiviral therapy with both ganciclovir and foscarnet.
Conclusion. PVAN with concurrent CMV infection in kidney transplant recipients
showed variable clinical courses including mortality. Further studies are needed to
elucidate the inﬂuence of PVAN on the pathogenesis of CMV infection.