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Abstract: TH-PO861

Cytomegalovirus-Associated Pulmonary Embolism

Session Information

Category: Transplantation

  • 2102 Transplantation: Clinical


  • Kassim, Mohamed J., University of Minnesota Twin Cities School of Medicine, Minneapolis, Minnesota, United States
  • Spong, Richard S., University of Minnesota Twin Cities School of Medicine, Minneapolis, Minnesota, United States

Thromboembolism has been associated with acute CMV infection or reactivation in transplant recipients. Here, we present a case of a young man with no apparent risk of a hypercoagulable state who developed a PE in the setting of a significant CMV viral load.

Case Description

The patient is a 24-year-old male with a PMH of ESRD secondary FSGS, status post LDKT 7 months earlier. Induction was with anti-TG and basiliximab, follow by maintenance immunosuppression. He was CMV and EBV IgG antibody positive at the time of transplant and did receive 3 months of prophylaxis with oral valganciclovir. The patient presented to the hospital with complaints of gastrointestinal symptoms, dyspnea, and pleuritic chest pain.He reported having watery diarrhea for over 10 days, as well as nausea, vomiting, chills, fatigue and an episode of fever to 102F. A few days prior to his admission, he developed pleuritic chest pain and dyspnia. Physical examination was unremarkable except for dry mucous membranes and low BP, which improved with volume resuscitation. CT angiogram revealed a right middle, lower segmental and sub-segmental pulmonary emboli with partial occlusion. Stool studies were normal. CMV PCR of the blood was positive with more than 222,000 copies. EBV PCR blood was negative. He was started on a therapeutic heparin drip and was transitioned to Apixaban prior to discharge. Induction dosing of IV ganciclovir was started for CMV viremia which continued upon discharge.


The etiology of acute PE in our patient is believed to be triggered by the CMV infection. It has been reported in the medical literature that CMV can cause endovascular injury that can lead to thrombus formation and embolization. CMV reactivation is mostly seen in CMV discordant recipients (D+/R-), however, CMV reactivation can occur, albeit less frequently and at a lower viral load in seropositive recipients, as in this case. Latent CMV has been found on the endothelial cells of both venous and arterial vascular walls. It has been postulated that CMV-infected endothelial cells increase the expression of tissue factor II, which is involved in hemostasis and thrombus formation. CMV and other enveloped viruses have phosphatidylserine-like procoagulant activity on their surfaces which predispose to thrombus formation. In conclusion, acute CMV infection is a risk factor for thrombosis in transplant recipients and immunocompromised patients.