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Abstract: SA-PO473

A Severe Case of Cyclophosphamide Induced Hyponatremia

Session Information

Category: Fluid‚ Electrolyte‚ and Acid-Base Disorders

  • 1002 Fluid‚ Electrolyte‚ and Acid-Base Disorders: Clinical


  • Alonso, Shawn, University of Miami School of Medicine, Miami, Florida, United States
  • Valdes Sanchez, Chavely, University of Miami School of Medicine, Miami, Florida, United States
  • Anam, Raman, University of Miami School of Medicine, Miami, Florida, United States
  • Waheed, Ahmed A., University of Miami School of Medicine, Miami, Florida, United States

Mild to moderate hyponatremia is a known complication of cyclophosphamide (CY) which has been reported in numerous case reports2,3 and retrospective analysis.1 Here we present a case of CY-induced acute severe hyponatremia in a patient with diffuse large B-cell lymphoma.

Case Description

Patient is a 37-year-old female with a recent diagnosis of diffuse large B cell lymphoma on etoposide, prednisone, oncovin, cyclophosphamide-hydroxydaunorubicin (EPOCH). After the EPOCH, she received 20mg/kg of intravenous CY and instructions to drink copious amounts of water. The following day, the patient was lethargic with a headache and nausea. Labs revealed sodium of 118mmol/L down from 140mmol/L the day before, with a serum osmolality of 231mOsm/L, urine osmolality of 541mOsm/L, and urine sodium of 175mmol/L. Hypertonic saline was initiated nevertheless the patient suffered a seizure and was taken to the ICU. Despite multiple hypertonic saline boluses, the sodium continued to drop to a nadir of 110mmol/L. Conivaptan was initiated, and the sodium gradually increased to 127mmol/L. The patient was discharged neurologically intact on salt tabs.


Severe hyponatremia is a life-threatening complication of CY and it can develop rapidly. The potential mechanisms behind this complication may be either a substantial release of antidiuretic hormone (ADH), the enhanced action of ADH on the kidneys, or both. However, more recent studies have reported direct toxic effect of CY metabolites on the collecting tubules, as opposed to an increase in endogenous ADH.4 Prior reports have also concluded that this adverse effect can occur with both high (>40 mg/kg) and low dose (<20 mg/kg) CY.1,2,3 The degree of hyponatremia is also likely influenced by an increased free water intake, which is recommended prior to CY administration to reduce the risk of cystitis. Symptoms like pain and nausea which are known to increase the release of endogenous ADH can also contribute to the degree of hyponatremia.5 This case not only highlights the importance of being aware of this adverse effect but also suggests that there may be a potential need for a standardized protocol to monitor these patients given the danger of acute hyponatremia. The protocol could include patient education, frequent monitoring of serum sodium following the administration of CY, as well as treating any symptoms known to promote ADH release.