Abstract: SA-PO0612
Refractory Hypomagnesemia in Gitelman Syndrome Improved After SGLT2 Inhibitor Therapy
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
- Sandoval, Martin, The University of Texas Health Science Center at San Antonio, San Antonio, Texas, United States
- Nassar, Tareq Issa, The University of Texas Health Science Center at San Antonio, San Antonio, Texas, United States
Introduction
Gitelman syndrome is an inherited salt-wasting tubulopathy caused by mutations such as SLC12A3, characterized by hypokalemic metabolic alkalosis and hypomagnesemia. Hypomagnesemia is often refractory to supplementation. SGLT2 inhibitors have been associated with increased serum magnesium, although their utility in Gitelman syndrome has not been established.
Case Description
A middle-aged male with genetically confirmed Gitelman syndrome due to compound heterozygous pathogenic variants in SLC12A3 had persistent hypomagnesemia despite aggressive therapy. His regimen consisted of amiloride 10 mg daily, potassium chloride 80 mEq three times daily, and high-dose oral magnesium supplementation (up to magnesium oxide 800 mg four times daily, later magnesium glycinate up to 2000 mg four times daily), which was limited by gastrointestinal intolerance. Over 5 years, serum magnesium remained persistently low (1.2–1.4 mg/dL), with associated hypokalemia (K 3.1–3.5 mEq/L) and metabolic alkalosis (bicarbonate 29–33 mEq/L). Given refractory hypomagnesemia, dapagliflozin was initiated. Following treatment, serum magnesium increased from 1.2 mg/dL to 1.6 mg/dL.
Discussion
This case highlights a clinically meaningful increase in serum magnesium following SGLT2 inhibitor initiation in a patient with genetically confirmed Gitelman syndrome. The mechanism is likely multifactorial. SGLT2 inhibition augments proximal sodium and water reabsorption, which may enhance passive paracellular magnesium uptake and reduce distal tubular flow and magnesium delivery to the distal nephron, where reabsorption is impaired. Although the primary defect in Gitelman syndrome is Na-Cl cotransporter dysfunction, upstream modulation may partially mitigate magnesium wasting. This observation supports consideration of SGLT2 inhibitors as an adjunctive option for refractory hypomagnesemia in inherited tubulopathies.
Acknowledgment
The authors acknowledge the support of the UT Health San Antonio Internal Medicine Residency Program and Division of Nephrology.