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Kidney Week

Abstract: TH-PO599

Everything Comes Down to Poo

Session Information

  • Trainee Case Reports - II
    October 25, 2018 | Location: Exhibit Hall, San Diego Convention Center
    Abstract Time: 10:00 AM - 12:00 PM

Category: Trainee Case Reports

  • 1802 Transplantation: Clinical

Authors

  • Mahajan, Kapil, UT Health Houston, Stafford, Texas, United States
  • Machado, Shana M., UT-Houston Nephrology, Houston, Texas, United States
Introduction

Use of immunosuppressive agents can predispose transplant recipients to a variety of side effects like malignancies, infections, anemia. Anemia in post transplant period can be from several causes including delayed graft function, blood loss, infections. Here we present a case of anemia from Hemphophagocytic lymphocytosis (HLH) caused by Cytomegalovirus (CMV) colitis in a patient with negative CMV viremia

Case Description

A 54 yom was admitted for symptomatic anemia without active source of bleeding. He had a history of deceased donor renal transplant, CMV Donor negative/Recipient positive and EBV Donor positive/Recipient positive, complicated by delayed graft function. He had a history of chronic anemia, unresponsive to Epogen therapy. Bone marrow biopsy was done which demonstrated hemophagocytosis and atypical erythroblasts possibly related to viral infection. Immunostains for Parvovirus, EBV, CMV were negative. Due to RBC hypo-proliferation as well as development of diarrhea, he was empirically started on IV ganciclovir for possible CMV colitis. He underwent colonoscopy with colon biopsy demonstrating distortion, increased chronic inflammatory cells, crypt atrophy, focal crypt abscess. Immunoperoxidase staining was positive for CMV. The etiology of patient’s hemophagocytosis was from non-disseminated CMV. He was discharged home on oral valgancyclovir as well as outpatient clinic follow up

Discussion

Post transplant anemia can be due to medication side effects, frequent phlebotomy tests, slow graft function, viral infection. HLH is a syndrome of excessive inflammation and tissue destruction due to exaggerated immune response. Primary HLH is caused by a genetic mutation and secondary HLH occurs in autoinflammatory and autoimmune disease, lymphoma, viremia, iatrogenic immunosuppression. It is diagnosed if there is a mutation in a known causative gene or if at least 5 of 8 diagnostic criteria are met: fever,, splenomegaly, cytopenia involving > 2 cell lines, hypertriglyceridemia or hypofibrinogenemia, biopsy proven hemophagocytosis, low or absent natural killer cell activity, elevated serum ferritin, elevated CD25 levels. The pathogenesis of HLH is not well understood. Impairment of Natural killer-cell (NK-cell) function caused by viral infections can lead to persistent activation of macrophages and production of cytokines. When HLH is triggered by a viral infection, treatment of the underlying viremia is recommended