Kidney Week

Abstract: SA-PO0611

Severe Hypomagnesemia Causing Torsades de Pointes in Type 1 Diabetes: A Novel Role for SGLT2 Inhibition

Session Information

• Fluid, Electrolyte, and Acid-Base Disorders: Case Reports - 2
  October 24, 2026 | Location: Exhibit Hall A, 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

• Colón, Alexandra M., Universidad de Puerto Rico Recinto de Ciencias Medicas, San Juan, Puerto Rico

Alexandra M. Colón, MD

• Pico-Ramirez, Alexandra C., Universidad de Puerto Rico Recinto de Ciencias Medicas, San Juan, Puerto Rico

Alexandra C. Pico-Ramirez, MD

• Ocasio Melendez, Ileana E., Universidad de Puerto Rico Recinto de Ciencias Medicas, San Juan, Puerto Rico

Ileana E. Ocasio Melendez, MD, FASN

• Vega-Colon, Jesus Daniel, Universidad de Puerto Rico Recinto de Ciencias Medicas, San Juan, Puerto Rico

Jesus Daniel Vega-Colon, MD

Introduction

Severe hypomagnesemia is a potentially life-threatening electrolyte disorder associated with cardiac arrhythmias, including torsades de pointes. Renal magnesium wasting represents a difficult therapeutic challenge when conventional supplementation and potassium-sparing agents fail. Emerging evidence suggests that sodium-glucose cotransporter-2 (SGLT2) inhibitors may improve magnesium handling, though data remain limited, particularly in patients with type 1 diabetes mellitus.

Case Description

Case of a 24-year-old male with type 1 diabetes mellitus who presented with complaints of episodes of chest discomfort, palpitation and dizziness which had been occurring for the past months. During an emergency department evaluation, he developed polymorphic ventricular tachycardia (torsades de pointes) which resolved with magnesium administration. Laboratories at that time were remarkable for adequate renal function with severe hypomagnesemia. The patient then had multiple visits to emergency departments due to similar complaints and was always found with severe hypomagnesemia requiring IV repletion. He denied the presence of polyuria or persistent diarrhea. Further evaluation was remarkable for elevated urine magnesium levels with a fractional excretion of 13% consistent with renal magnesium wasting. Genetic testing for hereditary renal tubular disorders was negative. The patient was started on amiloride therapy without improvement in magnesium levels. He was requiring approximately 4 grams of intravenous magnesium sulfate, as well as multiple magnesium oral formulations, without improvement in magnesium levels which remained 1-1.3 mg/dL. After discussion with Endocrinology service, he was started on SGLT2 inhibitor therapy with Empagliflozin. Within 5 days of therapy, magnesium levels remained above 1.5mg/dL with use of oral magnesium supplements but no longer requiring intravenous replacements.

Discussion

This case highlights type 1 diabetes mellitus as a potential contributor to refractory renal magnesium wasting and underscores the emerging therapeutic role of SGLT2 inhibitors as adjunctive therapy in severe hypomagnesemia, especially in patients with life-threatening arrhythmia risk. The patient’s rapid stabilization following initiation of empagliflozin supports a potential role for SGLT2 inhibition in enhancing renal magnesium conservation.