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Abstract: SA-PO175

Drug (Carfilzomib)-Induced Atypical Hemolytic Uremic Syndrome (aHUS)

Session Information

Category: Onconephrology

  • 1700 Onconephrology

Authors

  • Pariya, Fnu, SUNY Downstate Health Sciences University, New York City, New York, United States
  • Sasidharan, Sandeep Raja, SUNY Downstate Health Sciences University, New York City, New York, United States
  • Jatoi, Tahir Ahmed, SUNY Downstate Health Sciences University, New York City, New York, United States
  • Azhar, Muhammad, Kings County Hospital Center, Brooklyn, New York, United States
  • Puri, Isha, Kings County Hospital Center, Brooklyn, New York, United States
  • Mallappallil, Mary C., Kings County Hospital Center, Brooklyn, New York, United States
  • Abushawer, Mohammad Waleed, SUNY Downstate Health Sciences University, New York City, New York, United States
Introduction

MM, the second most common hematologic malignancy, accounts for 2.1% of all cancer deaths (1). TMA is a potentially organ and life-threatening condition affecting patients with MM. Risk for TMA in MM is from both the disease and drug used to treat (2). We present an elderly man with refractory MM on Carfilzomib who developed aHUS.

Case Description

60-year-old male with history of prostate cancer in remission, refractory IgG Lambda chain associated MM, and was receiving chemotherapy with Carfilzomib presented with yellow productive cough for 3 days with fever and chills. On exam, Pt was febrile to 102 F, HR >100, and has rhonchi on lung fields. Labs showed Creatinine at 3.38 mg/dL (baseline 1.1mg/dl), WBC 10.57 K/uL with bands, Platelets 51K/uL and influenza A positive. CXR showed bibasilar opacities. The peripheral smear showed schistocytes with elevated LDH 795 U/L. ADAMS13 was negative and pt was diagnosed with aHUS. Patient was initiated on plasmapheresis followed by intermittent HD as the patient became oliguric with worsening renal functions. He was started on eculizumab after appropriate vaccinations. He had improvement in hematology labs but renal functions did not improve and remained dependent on iHD.

Discussion

TMAs in MM patients incur a high mortality risk with long-term morbidity like kidney failure as seen in our patient. MM- related TMA is poorly understood but thought to be due to VWF dysfunction mediates thrombotic thrombocytopenic purpura (TTP) (3), and uncontrolled complement activation mediates atypical hemolytic uremic syndrome (aHUS)(4). So Eculizumab, a complement inhibitor, is used with good results as in our patient but has not been studied as well. Influenza-associated TMA has been reported (5) which could be a trigger in our patient like other Carfilzomib TMAs (6, 7). It may be prudent to investigate if these patients need more frequent influenza vaccination. We report this case of TMA in MM especially with proteasome inhibitors to increase awareness for early detection and treatment thus can prevent morbidity and mortality.