M. Mayr et al., Polyomavirus BK nephropathy in a kidney transplant recipient: Critical issues of diagnosis and management, AM J KIDNEY, 38(3), 2001, pp. NIL_78-NIL_84
Diagnosis of polyomavirus BK nephropathy and treatment by low-dose immunosu
ppression may be optimized by using surrogate markers, such as the detectio
n of viral inclusion bearing cells in the urine and polyomavirus BK DNA in
plasma by polymerase chain reaction. These markers were used prospectively
in the management of a 44-year-old woman and led to the diagnosis of polyom
avirus BK nephropathy at an early stage. The management was complicated by
the concurrence of acute allograft rejection. Two treatment steps were init
iated: antirejection therapy consisting of methylprednisolone for 3 days fo
llowed by lowering of the maintenance immunosuppression. This treatment res
ulted in a return of the serum creatinine concentration to the baseline of
1.6 mg/L, clearance of polyomavirus BK from plasma, and disappearance of vi
ral inclusion bearing cells from the urine. After 2 months of stable allogr
aft function, a control biopsy confirmed the resolution of polyomavirus BK
nephropathy. Histologic signs of acute interstitial rejection were found an
d preemptively treated by methylprednisolone without altering the baseline
regimen. Allograft function remained stable without evidence of recurrent p
olyomavirus BK nephropathy. This case shows the value of surrogate markers
used in a prospective fashion for diagnosis 'and management of polyomavirus
BK nephropathy with concurrent rejection.