Impact of SGLT2 Inhibitors on Magnesium in Kidney Transplant Patients with and Without Diabetes

Magnesium (Mg<sup>2+</sup>) is essential for cardiovascular and metabolic health, yet hypomagnesemia is common in kidney transplant recipients (KTRs) due to immunosuppressive therapy and renal dysfunction. Oral Mg<sup>2+</sup> supplementation is often ineffective due to poor absorption and side effects. Sodium-glucose cotransporter 2 inhibitors (SGLT2i) have been shown to increase serum Mg<sup>2+</sup> in chronic kidney disease, but their effects in KTRs, particularly patients without diabetes, remain unclear. This observational study assessed 63 KTRs treated with dapagliflozin, analyzing the serum Mg<sup>2+</sup> levels at baseline and after 3 and 6 months. The hypomagnesemia prevalence, associations with oral supplementation, diabetes status, and diuretic use were evaluated. The results showed a significant Mg<sup>2+</sup> increase with SGLT2i therapy, reducing hypomagnesemia regardless of the diabetes status. Oral supplementation did not correlate with improved Mg<sup>2+</sup> levels, reinforcing its limited efficacy. Additional benefits included reductions in the body weight, blood pressure, and serum urate without compromising graft function. SGLT2i may offer a novel approach to managing hypomagnesemia in KTRs, potentially reducing the reliance on ineffective supplements while providing renal and cardiovascular benefits. Further research is needed to confirm these findings and elucidate the underlying mechanisms.

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Publication Details

Journal
International Journal of Molecular Sciences
Published
2025-03-22
DOI
https://doi.org/10.3390/ijms26072904
Citations
2
Primary Topic
Magnesium in Health and Disease
Type
article
Field-Weighted Citation Impact
2.24
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article

Impact of SGLT2 Inhibitors on Magnesium in Kidney Transplant Patients with and Without Diabetes

Candida Iacuzzo, Renata Angela Di Pietro, Nicoletta Vecchione, Carmine Secondulfo et al.
2 citations
International Journal of Molecular Sciences
Magnesium in Health and Disease
2.24
article

Impact of SGLT2 Inhibitors on Magnesium in Kidney Transplant Patients with and Without Diabetes

Candida Iacuzzo, Renata Angela Di Pietro, Nicoletta Vecchione, Carmine Secondulfo, Massimo Círillo, Maria Amicone, Giancarlo Bilancio, Luca Apicella, Sarah Hamzeh, A Pisani, Domenico Russo
article en
2 citations

Abstract

Magnesium (Mg<sup>2+</sup>) is essential for cardiovascular and metabolic health, yet hypomagnesemia is common in kidney transplant recipients (KTRs) due to immunosuppressive therapy and renal dysfunction. Oral Mg<sup>2+</sup> supplementation is often ineffective due to poor absorption and side effects. Sodium-glucose cotransporter 2 inhibitors (SGLT2i) have been shown to increase serum Mg<sup>2+</sup> in chronic kidney disease, but their effects in KTRs, particularly patients without diabetes, remain unclear. This observational study assessed 63 KTRs treated with dapagliflozin, analyzing the serum Mg<sup>2+</sup> levels at baseline and after 3 and 6 months. The hypomagnesemia prevalence, associations with oral supplementation, diabetes status, and diuretic use were evaluated. The results showed a significant Mg<sup>2+</sup> increase with SGLT2i therapy, reducing hypomagnesemia regardless of the diabetes status. Oral supplementation did not correlate with improved Mg<sup>2+</sup> levels, reinforcing its limited efficacy. Additional benefits included reductions in the body weight, blood pressure, and serum urate without compromising graft function. SGLT2i may offer a novel approach to managing hypomagnesemia in KTRs, potentially reducing the reliance on ineffective supplements while providing renal and cardiovascular benefits. Further research is needed to confirm these findings and elucidate the underlying mechanisms.

International Journal of Molecular SciencesVol. 26(7)
University of Salerno (IT), Ospedali Riuniti San Giovanni di Dio e Ruggi d'Aragona (IT), University of Naples Federico II (IT)
Good health and well-being
Openalex Percentile: Top 15%
Magnesium in Health and Disease
2.24
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