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Abstract: TH-PO075

Plasmapheresis as Adjunctive Treatment for Life-Threatening Rituximab-Induced Acute Respiratory Distress Syndrome

Session Information

Category: Acute Kidney Injury

  • 102 AKI: Clinical, Outcomes, and Trials


  • Yang, Christopher, University of Colorado Anschutz Medical Campus, Aurora, Colorado, United States
  • Bansal, Anip, University of Colorado Anschutz Medical Campus, Aurora, Colorado, United States

Rituximab is a monoclonal antibody targeted against the B-cell surface antigen CD20. It is used as therapy for a variety of conditions including hematologic malignancies and autoimmune diseases. Use of rituximab has been associated with hypersensitivity reactions (HSR) which can be classified as infusion-related, cytokine-release, type I (IgE/non-IgE), mixed, type III, and type IV reactions. While rituximab is typically associated with largely benign infusion reactions, it occasionally leads to serious type I reactions, which can cause life-threatening anaphylaxis. Rituximab can cause lung toxicity due to immediate hypersensitivity, via cytokine release and by a delayed HSR. We report the management of a patient with severe shock and ARDS attributed to a mixed HSR to rituximab infusion, which improved with plasmapheresis.

Case Description

A thirty-year old woman with myasthenia gravis (MG) was admitted with an acute exacerbation of MG after missing her maintenance dose of rituximab. She was initially treated with five sessions of plasmapheresis without any complications. Subsequently, she was treated with rituximab, per the standard protocol. Several hours after her rituximab infusion, she developed refractory shock, hypoxia, and hemoconcentration (Hgb 12 to 17 g/dl). Despite treatment with high dose steroids and broad-spectrum antibiotics, she rapidly developed ARDS requiring mechanical ventilation, oliguric acute kidney injury, and severe lactic acidosis. Her echocardiogram showed normal cardiac function and infectious work-up was ultimately negative. She was treated with one additional session of plasmapheresis to facilitate elimination of rituximab based on prior case reports. She subsequently had rapid improvement in clinical parameters with resolution of shock in three days, resolution of AKI soon after and extubation after six days.


Severe HSR, while rare, can be a potentially fatal adverse effect of rituximab. There is no well-described treatment of this reaction. We describe a case with rapid improvement after one treatment of adjunctive plasmapheresis. With the widespread use of rituximab for a variety of conditions, clinicians need to be aware regarding the diagnosis and management of the spectrum of HSRs associated with this drug.