Sodium-Glucose Cotransporter 2 Inhibitors and Management of Refractory Hypomagnesemia Without Overt Urinary Magnesium Wasting: A Report of 2 Cases
Shah CV, Robbins TS, Sparks MA
Kidney medicine · 19 citations
How it was studied
- Design
- Case report (indexed by PubMed)
- Studied in
- People
- Main outcome
- Health markers and function
Who paid for it
- Funding
- Independent funding
Based on full-text disclosure statement.
Publication
- Published
- 2022-08-11 · Kidney Med · vol. 4 · issue 10 · p. 100533
- Publisher
- Elsevier BV
- Cited
- 22 citations · more than 86% of similar papers · 2.0× the field average
- References
- 15 works
- Access
- Open access (journal) · CC-BY-NC-ND
- Research areas
- Magnesium in Health and Disease · Parathyroid Disorders and Treatments · Potassium and Related Disorders
- Keywords
- Hypomagnesemia, Internal medicine, Magnesium, Medicine, Magnesium deficiency (plants), Endocrinology, Urinary system, Wasting, Diabetes mellitus, Hypermagnesemia, Chemistry
3 authors
From US
- Chintan Vimalkumar Shah · correspondingUniversity of Florida
- T. Scott RobbinsDuke University; Durham VA Health Care System
- Matthew A. SparksDuke University; Durham VA Health Care System
Abstract
Sodium-glucose cotransporter 2 (SGLT2) inhibitor have become widely used in patients with diabetes, heart failure, and kidney disease to improve clinical outcomes and diminish hospitalizations. They have also been associated with increased serum magnesium levels in patients with type 2 diabetes. The use of SGLT2 inhibitors resulted in improved magnesium homeostasis in a series of patients with refractory hypomagnesemia with urinary magnesium wasting. However, the role of SLGT2 inhibitors in patients with hypomagnesemia without urinary magnesium wasting remains unexplored. We report 2 cases with refractory hypomagnesemia without significant urinary magnesium wasting and dramatically improved serum magnesium levels after the initiation of SGLT2 inhibitors. Case 1 achieved independence from weekly intravenous magnesium infusions and reached sustainably greater serum magnesium levels with decreased oral magnesium supplementation and increased urinary fractional excretion of magnesium. Case 2 demonstrated improved serum magnesium levels with reduced oral magnesium supplementation without significant reduction in urinary fractional excretion of magnesium. These findings not only expand the use of SGLT2 inhibitors but also open the door for further studies to better understand the pathophysiology of how magnesium homeostasis is altered with inhibition of SGLT2.
Abstract via Europe PMC. Copyright remains with the authors or publisher (CC BY-NC-ND).
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