Abstract: TH-PO1061
SGLT2 Inhibitor Use in Calcineurin Inhibitor-Associated Refractory Hypomagnesemia
Session Information
- Transplantation: Clinical - Outcomes, Malignancy, and Pathology
October 22, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Transplantation
- 2002 Transplantation: Clinical
Authors
- Katta, Pravahika, Shasta Regional Medical Center, Redding, California, United States
- Shaikh, Sana J., UC Davis Health, Sacramento, California, United States
- Kaur, Harpreet, UC Davis Health, Sacramento, California, United States
Introduction
Tacrolimus-induced hypomagnesemia is a common complication after kidney transplantation, primarily caused by renal magnesium wasting. In some kidney transplant recipients, magnesium levels remain persistently low despite oral and intravenous replacement. Clinically significant hypomagnesemia may manifest as neuromuscular irritability (tremors, cramps, weakness) and cardiac arrhythmias, underscoring the importance of sustained magnesium repletion. Emerging data suggest sodium-glucose cotransporter-2 (SGLT2) inhibitors may improve serum magnesium by reducing urinary magnesium losses, though their role in tacrolimus-associated hypomagnesemia remains underdefined.
Case Description
We report a case of a 67-year-old Filipino female kidney transplant recipient maintained on tacrolimus-based immunosuppression who developed persistent hypomagnesemia after transplantation despite stable allograft function. Evaluation showed renal magnesium wasting,
with an elevated fractional excretion of magnesium (FEMg) of 5.9%, consistent with tacrolimus- induced tubular magnesium loss.
Her hypomagnesemia remained refractory to standard treatment, including high-dose oral magnesium supplementation, switch from magnesium oxide to magnesium glycinate for better bioavailability, dietary magnesium optimization, and intermittent intravenous magnesium
repletion.
Given persistent renal magnesium wasting, empagliflozin was initiated at 10 mg daily and later increased to 25 mg daily. Following initiation and dose escalation, serum magnesium levels improved. This was accompanied by reduced urinary magnesium excretion, with FEMg
decreasing from 5.9% to 2.9%, and decreased need for intravenous magnesium supplementation.
Discussion
This case highlights the potential role of SGLT2 inhibitors as adjunctive therapy for refractory tacrolimus-induced hypomagnesemia in kidney transplant recipients. Tacrolimus can impair tubular magnesium handling, leading to persistent urinary magnesium loss despite supplementation. In this patient, empagliflozin was associated with improved serum magnesium, reduced FEMg, and decreased intravenous magnesium requirements.
SGLT2 inhibition may improve magnesium homeostasis through effects on renal tubular electrolyte handling, although the precise mechanism remains uncertain. Further studies are needed to define efficacy, safety, dosing, and long-term outcomes SGLT2 inhibitors in this population.