Abstract

A 55-year-old man received a kidney transplantation in June 2008 (diabetic end-stage renal disease). Induction of immunosuppression consisted of basiliximab, methylprednisolone and mycophenolate mofetil. Maintenance therapy consisted of prednisone, mycophenolate mofetil and tacrolimus. In December 2008, a kidney biopsy was performed because of deteriorated kidney function and blood BK virus (BKV) replication (105.9 copies/mL). The biopsy showed prominent lymphocytic interstitial infiltrates. Tubulitis was inconspicuous (Figure 1A). Intranuclear inclusion bodies with ground-glass appearance and peripheral chromatin rimming could be seen in some tubular epithelial cells consistent with BKV infection (Figure 1B). No deposits were identified by immunofluorescence. Immunosuppression was reduced. Ten days after the biopsy, a contrast-enhanced CT scan was performed for intercurrent intestinal discomfort (no specific diagnosis made, with spontaneous recovery). The CT scan showed multiple wedge-shaped areas and streaky zones of lesser enhancement that extended from the papilla to the renal cortex (Figure 2). Ultrasonography performed the same day showed very similar abnormalities. The patient was afebrile. The urine dipstick showed no leucocytes, no red blood cells and no nitrite. The C-reactive protein was 5.5 mg/dL (N <5 mg/dL) and serum creatinine was stable. The patient was treated with ceftriaxone and amikacine in the emergency department, because of the imaging findings. The next day, urine analysis showed no white cells and a culture yielded no bacteria. Antibiotic therapy was discontinued. No other cause than BKV nephropathy (BKN) was retrospectively found to explain the ‘radiological nephritis’. Six months after the reduction of immunosuppression, the plasma BK viral load decreased considerably (102.3 copies/mL) and serum creatinine returned to pre-BKN value. Ultrasonography returned to normal, explaining why a contrast CT scan was not performed as control. To our knowledge, no radiological description of BKN has been made to date. In our case, it was seen as a nonspecific nephritis, the topography of which was consistent with the pathophysiology of BKN.

Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call