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Abstract: SA-PO703

Correction of Refractory Hypomagnesemia by SGLT2 Inhibitor

Session Information

Category: Fluid, Electrolytes, and Acid-Base Disorders

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


  • Zhao, Jinhua, VA Northeast Ohio Healthcare System, Cleveland, Ohio, United States

Correcting hypomagnesemia can be difficult due to limited gastrointestinal (GI) absorption of oral Magnesium (Mg) supplements, diarrhea with high dose supplement, and lack of effective agents to decrease renal losses. The reported prevalence of hypomagnesemia is 14%-48% in type 2 diabetic patients. With the growing use of Sodium-Glucose Cotransport 2 Inhibitors (SGLT2i) for cardiac protection, renal protection and proteinuria, etc., post hoc analyses have shown the association of SGLT2i use with increased blood magnesium. A few clinical case reports also demonstrated improvement of hypomagnesemia with SGLT2i. The mechanism by which SGLT2i correct hypomagnesemia is unclear.

Case Description

74 year old male passed out at a restaurant 4 years ago, he was found to have serum magnesium (Mg) of 0.8mg/dL. Mg supplement was started. He again had severe hypomagnesemia when evaluated for photophobia. Since then he also got intermittent iv Mg. Mg was maintained at 1.4-1.6 mg/dL. Other medical issues include type 2 diabetes, hypertension. No chronic nausea, vomiting; no PPI or diuretic use. He is well nourished, not alcoholic. HbA1c was 6’s - 8’s. eGFR was >60 cc/min, no microalbuminuria.

Work-up showed renal Mg wasting as fractional excretion of Magnesium (FEMg) was 6% when plasma Mg was 1.6 mg/dL in 2/2022. SGLT2i (empagliflozin 12.5mg daily) was added in March 2022, plasma Mg increased to 1.8 mg/dL 1 month later, then to 2.0 mg/dL 3 months later. Plasma Mg has been remain at 2.0 mg/dL over the following 10 months.

The increase of plasma Mg from 1.6 to 2.0 mg/dL was associated with decrease of FEMg from 6% to 3%. After plasma Mg stablized at 2.0 mg/dL, FEMg was 13% and 10% on 2 occasions. See Table.


GI loss or renal losses are the two major etiologies of hypomagnesemia. This patient had refractory hypomagnesemia despite oral and intermittent iv supplements. His elevated FEMg in presence of hypomagnesemia was consistent with renal wasting. The initiation of SGLT2i rapidly normalized plasma Mg. While plasma Mg remains at 2.0 mg/dL in the following months, the FEMg increased again. This increased most likely represents appropriate renal handling in responding to GI Mg intake.

Mg (mg/dL)
FEMg (%)6631310