ASN's Mission

To create a world without kidney diseases, the ASN Alliance for Kidney Health elevates care by educating and informing, driving breakthroughs and innovation, and advocating for policies that create transformative changes in kidney medicine throughout the world.

learn more

Contact ASN

1401 H St, NW, Ste 900, Washington, DC 20005

email@asn-online.org

202-640-4660

The Latest on X

Kidney Week

Abstract: SA-PO1279

Severe Hyponatremia After Mirvetuximab Soravtansine Therapy: A Case of Suspected Drug-Associated Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH)

Session Information

Category: Onconephrology

  • 1600 Onconephrology

Authors

  • Kashfi, Simon Adam, Donald and Barbara Zucker School of Medicine at Hofstra/Northwell, Hempstead, New York, United States
  • Bhuiyan, Md Refayat, Donald and Barbara Zucker School of Medicine at Hofstra/Northwell, Hempstead, New York, United States
  • Wanchoo, Rimda, Donald and Barbara Zucker School of Medicine at Hofstra/Northwell, Hempstead, New York, United States
  • Jhaveri, Kenar D., Donald and Barbara Zucker School of Medicine at Hofstra/Northwell, Hempstead, New York, United States
Introduction

Hyponatremia is a common electrolyte abnormality in oncology patients with multifactorial etiologies. Mirvetuximab soravtansine, an antibody-drug conjugate used in ovarian cancer, has rarely been associated with mild hyponatremia. Severe (grade 3–4) hyponatremia has not been previously well described.

Case Description

An 89-year-old woman with ovarian cancer, well controlled hypothyroidism, and hyperlipidemia presented with fatigue following a recent fall with head hematoma. She had initiated treatment with Mirvetuximab soravtansine and bevacizumab. Her last infusion was two weeks prior to admission, at which time serum sodium (Na) was 125 mmol/L. Baseline sodium prior to therapy was 135 mmol/L.

On presentation, serum sodium was 117 mmol/L, which further decreased to 114 mmol/L after 500 mL normal saline administration. Urine studies were consistent with SIAD (urine sodium 107 mmol/L, urine osmolality 427 mOsm/kg), with low uric acid (2.4 mg/dL). Repeat urine osmolality increased to 651 mOsm/kg. Imaging revealed bladder distention (>500 mL), and a Foley catheter was placed for urinary retention. Despite addressing potential contributors including trimethoprim-sulfamethoxazole and obstruction, hyponatremia persisted. Hypertonic saline and loop diuretics were administered with close monitoring to treat the hyponatremia. Adrenal insufficiency and hypothyroidism were ruled out. Cancer is under control on the current regimen.

Discussion

This case demonstrates severe hyponatremia consistent with SIADH in a patient receiving Mirvetuximab-based therapy. While hyponatremia has been reported with this agent, it is typically mild and uncommon, and grade 3–4 severity has not been previously described. Although alternative etiologies including malignancy-associated SIAD, medications, and urinary retention were considered, the temporal association with therapy initiation and progressive sodium decline raises concern for a potential drug-related effect.