LAUSR

B virus nephropathy (BKVN) is well described in renal allografts with the most consistent risk factor being overall degree of immunosuppression. BKVN in native kidneys is far less common and hitherto described most frequently in heart and hematopoietic cell transplant recipients. Native BKVN in a liver transplant recipient has been documented only once before in the literature; here, we report a second case. A 59-year-old Vietnamese-born man received an ABOincompatible orthotopic liver transplant for acute liver failure secondary to hepatitis B virus reactivation. Due to blood group incompatibility, his induction therapy was according to our standard protocol of pretransplant rituximab and posttransplant methylprednisolone, basiliximab, tacrolimus, and plasmapheresis. His maintenance immunosuppression was more intense than standard at our center consisting of prednisone 5 mg daily, mycophenolate mofetil 1000 mg BID, and tacrolimus with trough levels between 7 and 10 ng/mL, as he had a rebound in anti-B titer from 1:4 to 1:16 posttransplant. He had excellent graft function with no rejection, and his posttransplant serum creatinine had been 60 and 80 μmol/L and estimated glomerular filtration rate >90 mL/ min/1.73 m. He received hepatitis B prophylaxis with long-term entecavir. Twenty-two months posttransplant, he presented with diarrhea due to biopsy-proven cytomegalovirus colitis and acute kidney injury. Despite clinical improvement after intravenous ganciclovir and fluid resuscitation, his renal function remained significantly impaired with a creatinine level of 280 μmol/L (estimated glomerular filtration rate, 20 mL/min/1.73 m). He had no proteinuria or hematuria, and his renal ultrasound did not demonstrate any evidence of obstruction. A serum quantitative polymerase chain reaction test for BK virus was strongly positive with 754 976 copies/mL. A renal biopsy later confirmed severe BK nephropathy with considerable interstitial inflammation (Figure 1). His immunosuppression was reduced, and he was commenced on fortnightly cidofovir infusions. Recent studies have suggested a high prevalence of BK viremia and viruria among liver transplant recipients; however, there are conflicting data on their relationship with renal function. To date, there was only one other reported case of BKVN in a liver transplant recipient 7 years posttransplant who had received heavy immunosuppression to treat multiple rejection episodes. Little is known about the risk factors for the development of BKVN after liver transplant; however, both our patient and that previously reported are male, are older than 55 years, and have a history of greater than standard exposure to immunosuppression. In this case, the additional complication of cytomegalovirus colitis was also probably reflective of heavy immunosuppression used. As renal biopsy is not routinely performed in liver transplant patients with acute kidney injury, and with the perceived rarity of BKVN in this patient group, we suspect that BKVN is underrecognized. The optimal treatment of BKVN in native kidneys of recipients of organs other than kidneys is not known. The best available evidence supports a reduction in immunosuppression; however, other strategies, such as cidofovir and intravenous immunoglobulin, have also been used. Further studies are required to determine those liver recipients most at risk of developing BKVN and to investigate the role of renal biopsy in this group to assist in the timely detection ISSN: 0041-1337/20/1043-e83