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Abstract: FR-PO230

Erythrocytapheresis in the Management of Acute Sodium Nitrate Toxicity

Session Information

  • Pharmacology
    November 04, 2022 | Location: Exhibit Hall, Orange County Convention Center‚ West Building
    Abstract Time: 10:00 AM - 12:00 PM

Category: Pharmacology (PharmacoKinetics‚ -Dynamics‚ -Genomics)

  • 1900 Pharmacology (PharmacoKinetics‚ -Dynamics‚ -Genomics)


  • Ha, Nam, UVA Health, Charlottesville, Virginia, United States
  • Hughes, Parker K., UVA Health, Charlottesville, Virginia, United States
  • Kumar, Anubhav, UVA Health, Charlottesville, Virginia, United States

Sodium nitrate, a common food preservative, is increasingly implicated in suicide attempts. Nitrate oxidizes hemoglobin to methemoglobin, which has poor oxygen-binding capacity. At high concentrations, methemoglobinemia leads to cardiovascular collapse. We present a case of life-threatening methemoglobinemia following intentional sodium nitrate ingestion requiring erythrocytapheresis (RBC exchange) and arteriovenous extracorporeal membrane oxygenation (VA ECMO).

Case Description

A 27-year-old woman with a history of depression reported to emergency services that she had injected sodium nitrate into her abdomen. On arrival to the emergency department, she was unresponsive, cyanotic, hypotensive, and hypoxic to oxygen saturation of 75%. Methemoglobin level was 86%. She was given methylene blue, intubated with succinylcholine and started on vasopressor and ascorbic acid. Nephrology was consulted for RBC exchange and cardiothoracic surgery for possible serotonin syndrome after methylene blue administration. Patient underwent cannulation to begin VA ECMO. RBC exchange was begun via the ECMO circuit; 2200 mL of red cell volume was exchanged, and methemoglobin level decreased to 5.6%. The patient required no further apheresis therapy and was later decannulated from VA ECMO the next day and eventually transferred for psychiatric care.


Sodium nitrate ingestion induces cardiovascular collapse via smooth muscle relaxation, compromising venous return. Methemoglobin production occurs via nitrate-mediated oxidation of hemoglobin’s ferrous moiety to ferric, impairing oxygen binding and producing hypoxia. Methylene blue may be helpful to reduce ferric iron to ferrous but may be inadequate on its own in cases of extreme poisoning or cardiorespiratory symptoms. Rapid initiation of erythrocytaphresis may be life-saving in these situations, as observed in this case.