Late Presentation of Adenovirus-Induced Hemorrhagic Cystitis and Ureteral Obstruction in a Kidney-Pancreas Transplant Recipient

Abstract

We report a late presentation of adenovirus-induced renal allograft and bladder infection causing azotemia and hemorrhagic cystitis in a patient 5 years after simultaneous kidney-pancreas transplantation. Adenovirus has been increasingly recognized as a cause of morbidity and mortality in both solid organ and stem cell transplant recipients. We wish to emphasize the importance of early detection, as treatment options involve reduction of immunosuppression, followed by the addition of antiviral agents and supportive care.A denovirus causes 5% to 10% of all childhood febrile illnesses, and the immunocompetent host generally endures a mild, self-limited upper respiratory tract infection. Adenovirus then establishes latent infection in the lymphoepithelial tissues (1). In immunocompromised hosts, the clinical manifestations of adenovirus reactivation or de novo infection can range from asymptomatic to fatal. Adenovirus is identifi ed as a late complication of bone marrow transplantation with hemorrhagic cystitis, and it is increasingly recognized as a serious, though rare, adverse complication of solid organ transplantation. We describe a rare late presentation of hemorrhagic cystitis and signifi cant renal allograft dysfunction with ureteral obstruction in a patient who had undergone simultaneous kidney-pancreas transplantation (SKP) nearly 5 years earlier. With adenovirus detected in the urine, blood, and renal allograft, the patient was treated with reduction of immunosuppression, intravenous immunoglobulin, and cidofovir. Renal function did not improve despite treatment. Pancreas function, as in rare case reports, was preserved, suggesting tropism of the adenovirus. CASE DESCRIPTIONA 45-year-old African American woman had a past medical history of type 1 diabetes mellitus complicated by peripheral neuropathy, retinopathy, and end-stage renal disease. She underwent SKP in February 2009 and received daclizumab induction per protocol. Th e donor was a 2/6 human leukocyte antigen match, and both donor and recipient were cytomegalovirus positive. Th e transplant was complicated by cellular rejection of the kidney in March 2009 treated with Solu-Medrol and biopsy-proven pancreas rejection treated with 10 doses of muromonab-CD3. Renal function stabilized with a creatinine of 1.4 mg/dL. Maintenance immunosuppression included azathioprine 100 mg daily, prednisone 5 mg daily, and tacrolimus 4 mg twice daily.Five years after transplant, the patient presented with a 1-week history of fever, suprapubic pain, and nausea, with the development of hematuria 3 days later. She had presented to an emergency department for presumed urinary tract infection 3 days before admission and was treated with nitrofurantoin. However, she developed worsening hematuria and presented to the transplant clinic. She denied sick contacts and had been compliant with all medications. On examination, she had orthostatic hypotension and fever. She was pale and appeared acutely ill. Th e left lower quadrant and suprapubic area were tender without rebound...

Adenovirus-Associated Acute Interstitial Nephritis With Graft Survival and Novel Follow-Up Biopsy Findings Including Karyomegaly: A Case Series

“…Interestingly, all three cases identified in this case series also coincidentally involved ureteral foreign bodies (stones, stents) or ureteral manipulation shortly before the identification of AAIN. Clinically relevant adenoviruses are known to infect a multitude of organs in the body, but the B-type adenoviruses, in particular, have the propensity to infect the urinary tract and cause hemorrhagic cystitis, especially in immunosuppressed patients who recently received a solid organ transplant [ 2 , 3 , 11 ]. While the exact mechanism by which adenoviruses seed tubular epithelial cells and cause AAIN is unknown, it is feasible that the presence of a ureteral foreign body or external ureteral manipulation may raise the likelihood of ascending infection to the allograft from the bladder rather than hematologic spread from a primary gastrointestinal or respiratory infection.…”

Disseminated Adenovirus Infection After Combined Liver-Kidney Transplantation

“…We report a case of disseminated HAdV type 21 infection presenting 5 months after combined liver-kidney transplantation. Symptomatic HAdV infections are infrequently reported in adult SOT recipients (Hofland et al, 2004 ; Ison, 2006 ; Kozlowski et al, 2011 ; Storsley and Gibson, 2011 ; Sujeet et al, 2011 ; Dawood et al, 2014 ; Lachiewicz et al, 2014 ; Klein et al, 2015 ; Mehta et al, 2015 ; Saliba et al, 2017 ). An exception to this is the lung transplant population in whom community acquired asymptomatic viremia secondary to HAdV are not infrequent (Humar et al, 2006 ; Bridevaux et al, 2014 ), likely due to the uniqueness of the graft being in direct exposure to the outside environment.…”