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Internal Medicine

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A 55-year-old CMV seronegative woman with type 1 diabetes mellitus and end stage renal disease received a cadaveric renal allograft from a CMV positive donor five months prior. She is on valganciclovir prophylaxis.

She now presents with decreasing renal function despite increased immunosuppression with tacrolimus and prednisone given for suspected graft rejection. Tacrolimus levels are in the therapeutic range. Ultrasound did not show obstruction of the implanted kidney. You are consulted about possible infectious causes of renal failure. She is afebrile and routine urinalysis with bacterial culture is unremarkable.

Your preferred approach to establish the cause of the renal failure is which of the following:

  • 0% Quantitative urine PCR for BK virus

  • 0% Quantitative urine PCR for adenovirus

  • 0%Renal biopsy

  • 0% Blood for quantitative CMV viral load


The principal concern in this patient is possible BK virus nephropathy.

Although quantitative PCR of plasma or urine has been advocated for diagnosis, the most reliable diagnostic measure is demonstration of the characteristic basophilic inclusions in renal tubular cells on renal biopsy. Seeing these tubular cells in urine cytology, “decoy cells” is too common to be diagnostic, though absence of these cells suggests against the diagnosis.

BK, a polyoma virus, cannot be cultured by routine measures and large quantities can be found by PCR of urine from immunosuppressed patients without nephropathy. Blood may be positive for BK virus but cannot distinguish between BK nephropathy and rejection, which would be treated differently (reduction versus intensification of immunosuppression).

JC virus causes progressive multifocal leukoencephalopathy, not nephropathy. 

Adenovirus would not be expected to cause azotemia in renal transplant recipients.

CMV is extremely unlikely while on prophylaxis and very rarely causes kidney injury.

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