Abstract: FR-PO0602
A Tale of Two Patients with Acute Hyponatremia Following Cyclophosphamide: Case Reports and Pathophysiological Perspectives
Session Information
- Fluid, Electrolyte, and Acid-Base Disorders: Clinical - 2
November 07, 2025 | Location: Exhibit Hall, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Fluid, Electrolytes, and Acid-Base Disorders
- 1102 Fluid, Electrolyte, and Acid-Base Disorders: Clinical
Authors
- Jensen, Colton, The Johns Hopkins University School of Medicine, Baltimore, Maryland, United States
- Tamargo, Christina Lauren, The Johns Hopkins University School of Medicine, Baltimore, Maryland, United States
- Hanouneh, Mohamad A., The Johns Hopkins University School of Medicine, Baltimore, Maryland, United States
- Cervantes, C. Elena, The Johns Hopkins University School of Medicine, Baltimore, Maryland, United States
Introduction
Cyclophosphamide (CYC) can lead to both acute and chronic hyponatremia through central and kidney-related mechanisms. This report presents two cases of acute hyponatremia linked to CYC use.
Case Description
Case 1: A 70-year-old woman with myelodysplastic syndrome underwent preconditioning for an unrelated donor bone marrow transplant. Her regimen included intravenous (IV) CYC and within 24 hours of the CYC dose, she developed nausea and muscle spasms, with a rapid serum sodium drop from 139 to 118 mmol/L. Patient was euvolemic and workup was consistent with hypoosmolar hyponatremia due to SIADH (Fig 1). She was successfully treated with 3% saline, resulting in symptom resolution within hours and sodium normalization within 24 hours.
Case 2: A 61-year-old woman with multiple myeloma underwent IV CYC-based mobilization for autologous peripheral blood stem cell transplant. Within 24 hours of CYC administration, her serum sodium dropped from 141 to 118 mmol/L and she experienced a seizure. Patient’s volume status was normal, and workup supported the diagnosis of hypoosmolar hyponatremia linked to SIADH (Fig 1). She was treated with lorazepam and hypertonic saline, leading to rapid clinical improvement and sodium correction to 132 mmol/L.
Discussion
CYC can cause both acute and chronic hyponatremia through distinct mechanisms. Acute hyponatremia typically occurs shortly after high-dose IV CYC administration and is commonly due to SIADH, leading to inappropriate water retention from excess ADH (Fig 2). In contrast, chronic hyponatremia may result from prolonged use of oral CYC and is often attributed to ADH-independent upregulation of aquaporin-2 channels in the kidneys (Fig 2). Given these risks, close monitoring of serum sodium is essential in patients receiving CYC. Prompt recognition and treatment, particularly with hypertonic saline in acute cases, is critical to prevent severe complications such as cerebral edema.