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Kidney Week

Abstract: SA-PO704

The Drug that Keeps Giving: Hypomagnesemia Fixed by SGLT2 Inhibitor

Session Information

Category: Fluid, Electrolytes, and Acid-Base Disorders

  • 1102 Fluid, Electrolyte, and Acid-Base Disorders: Clinical

Authors

  • Abdallah, Ahmed, University of Arkansas for Medical Sciences, Little Rock, Arkansas, United States
  • Ayub, Fatima, University of Arkansas for Medical Sciences, Little Rock, Arkansas, United States
  • Elkalashy, Ahmed, University of Arkansas for Medical Sciences, Little Rock, Arkansas, United States
  • Hasan, Md Rajibul, Arkansas College of Osteopathic Medicine, Fort Smith, Arkansas, United States
  • Errabelli, Praveen K., Mayo Clinic Health System Albert Lea, Albert Lea, Minnesota, United States
  • Lathiya, Maulik, Mayo Clinic Health System Albert Lea, Albert Lea, Minnesota, United States
  • Singh, Manisha, University of Arkansas for Medical Sciences, Little Rock, Arkansas, United States
  • Karakala, Nithin, University of Arkansas for Medical Sciences, Little Rock, Arkansas, United States
  • Holthoff, Joseph H., University of Arkansas for Medical Sciences, Little Rock, Arkansas, United States
Introduction

Sodium-glucose cotransporter 2 (SGLT2) inhibitors are widely used in patients with kidney disease to improve clinical outcomes. They are known to increase serum magnesium levels. There are rare case reports of these helping treat hypomagnesemia with or without urinary losses of magnesium. We present a case report to add to this data in treating refractory hypomagnesemia with a significant improvement in serum magnesium levels.

Case Description

A 72-year-old frail woman with a past medical history of type 2 diabetes mellitus and gastric bypass surgery presented to the emergency department with complaints of worsening fatigue and refractory chronic hypomagnesemia. The patient had experienced generalized weakness, tremors, and reduced appetite for many months. The patient had known chronic hypomagnesemia, hypokalemia, hypocalcemia, and alkalosis, thus a concern for Gitelman syndrome. She was prescribed oral supplementations without significantly improving serum magnesium levels. Her home medications included metformin and pantoprazole.

At the time of presentation, the patient had normal vitals, though she was very frail, demented, and resting tremors in her hands. serum magnesium was 0.9 mg/dl. The pantoprazole was discontinued, and oral and intravenous magnesium supplementation was started with a slight improvement in the serum magnesium levels to 1.2 mg/dl. Next, amiloride was added. However, she developed diarrhea likely secondary to the magnesium salts, which added to her gastric losses and inability to tolerate oral repletion.
The fractional excretion of magnesium (FeMg) was 69% consistent with renal magnesium wasting, but the genetic tests for Gitleman came back negative. Subsequently, we added an SGLT2 inhibitor with marked improvement in serum magnesium levels to 2.3 mg/dl and complete resolution of tremors.

Discussion

In patients with significant urinary magnesium wasting, supplementation often fails to improve serum magnesium levels. Clinical trials have shown that SGLT 2 inhibitors can improve hypomagnesemia in diabetic patients with urinary magnesium wasting. However, data on their efficacy in nondiabetic patients with hypomagnesemia is scarce. SGLT2 inhibitors may be considered in patients with intractable hypomagnesemia, representing a possible new tool in this challenging clinical disorder.