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Carfilzomib-induced atypical haemolytic uraemic syndrome: a diagnostic challenge and therapeutic success
  1. Alicia Darwin1,
  2. Leonger Malpica2,
  3. Jugraj Dhanoa3 and
  4. Hamza Hashmi2,4
  1. 1Morsani College of Medicine, University of South Florida, Tampa, Florida, USA
  2. 2Department of Blood & Marrow Transplant and Cellular Immunotherapy, Moffitt Cancer Center, Tampa, Florida, USA
  3. 3Internal Medicine, University of Louisville, Louisville, Kentucky, USA
  4. 4Department of Hematology Oncology, Medical University of South Carolina, Charleston, South Carolina, USA
  1. Correspondence to Dr Hamza Hashmi; hamzahashmi87{at}


Haemolytic uraemic syndrome (HUS) is a thrombotic microangiopathy (TMA) that presents with renal insufficiency, thrombocytopaenia and microangiopathic haemolytic anaemia. Typical HUS is associated with Shiga toxin while atypical HUS (aHUS) is due to overactivation of the alternative complement pathway. aHUS has numerous causes, including drugs, with rare reports of carfilzomib, a proteasome inhibitor used in multiple myeloma, as causative agent. Cases vary in presentation, presenting a diagnostic challenge. Historically, TMAs were treated with plasma exchange. aHUS, however, is considered refractory to plasma exchange and best treated with eculizumab, a monoclonal antibody targeting C5, a terminal complement protein. We report a patient with history of multiple myeloma who presented with headaches, elevated blood pressure, petechiae, ecchymosis and haemolytic anaemia. His condition was determined to be carfilzomib-induced aHUS and he was successfully treated with eculizumab. Early detection and treatment of drug-induced aHUS is vital in reducing morbidity and mortality related to the condition.

  • haematology (drugs and medicines)
  • haematology (incl blood transfusion)
  • malignant and benign haematology
  • oncology

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  • Contributors AD: contributed to the writing and editing of report. LM: contributed to the writing and editing of report. JSD: contributed to the writing and editing of report. HH: contributed to the writing and editing of report. Patient was under the care of HH. Author team supervised by HH.

  • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

  • Competing interests None declared.

  • Patient consent for publication Obtained.

  • Provenance and peer review Not commissioned; externally peer reviewed.