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Abstract: FR-PO883

Adenovirus Allograft Nephropathy Mimicking Acute T Cell Rejection

Session Information

Category: Transplantation

  • 1802 Transplantation: Clinical


  • Alquadan, Kawther Farouk, University of Florida, Gainesville, Florida, United States
  • Zeng, Xu, University of Florida, Gainesville, Florida, United States
  • Koratala, Abhilash, University of Florida, Gainesville, Florida, United States

Adenovirus is associated with significant morbidity and mortality in renal transplant recipients and may even lead to the loss of allograft. Adenovirus nephropathy can be confused with acute cellular rejection as illustrated in our case. As the management of these two entities is completely different, clinical correlation is crucial.

Case Description

A 33-year-old African American woman with a history of ESRD status post deceased donor kidney transplantation was admitted for acute kidney injury (AKI) with a Scr of 8mg/dL (baseline 1.3). Her pre-transplant CPRA was 29%, received Alemtuzumab for induction immunosuppression (IS) followed by mycophenolate mofetil, tacrolimus and prednisone for maintenance. Her post-transplant course was complicated by BK viremia that resolved with reduction in IS. This time, BK virus serology was negative and she was given methylprednisolone 1 gram/day for 3 days for suspected rejection. She later developed fever and hematuria and clinically deteriorated despite receiving broad-spectrum antibiotics. Blood cultures remained negative. Allograft biopsy demonstrated severe interstitial inflammation with T cells, mononuclear cells and plasma cells with severe tubulitis [Figure]. Immunohistochemistry staining was negative for adenovirus but serum adenovirus PCR was positive with 10 million copies/ml. Her respiratory status worsened and CT scan of the chest showed tree-in-bud nodular opacities. Adenovirus PCR was positive in BAL and in the urine suggestive of adenovirus pulmonary and renal allograft involvement. Mycophenolate was held and she received treatment with intravenous immunoglobulin and cidofovir. Patient clinically improved and Scr was 1.5mg/dl at discharge. A repeat biopsy at follow-up visit was negative for rejection, showed mild interstitial fibrosis and tubular atrophy with no glomerulosclerosis [Figure].


High index of suspicion for adenovirus infection is required in renal graft dysfunction, especially in the setting of hematuria. Histology can mimic acute rejection, which creates a diagnostic dilemma. Tissue adenovirus immunostains, though usually reliable, may not be always positive like in our case.