Magnesium in Diabetes Mellitus and Diabetic Kidney Disease
8 affiliations
- 1Unit of Nephrology and Dialysis, Department of Clinical and Experimental Medicine, University of Messina, 98125 Messina, Italy
- 2Unit of Nephrology and Dialysis, Ospedali Riuniti Villa Sofia Cervello, 90146 Palermo, Italy
- 3Unit of Geriatric Medicine, Italian National Research Center on Aging (IRCCS INRCA), 87100 Cosenza, Italy
- 4PhD Program in Molecular and Clinical Medicine, University of Palermo, 90100 Palermo, Italy
- 5Department of Nephrology and Dialysis, Maggiore Nino Baglieri Hospital, 97015 Modica, Italy
- 6Department of Clinical and Experimental Medicine, University Hospital of Messina, 98125 Messina, Italy
- 7Department of Pharmacy, Health and Nutritional Sciences, University of Calabria, Rende, 87036 Cosenza, Italy
- 8Department of Renal Medicine, University Hospitals of Coventry and Warwickshire, Coventry CV2 2DX, UK
Abstract
Magnesium is a cofactor in cellular energy metabolism and insulin signaling, with recognized effects on vascular tone and cardiac electrophysiology. Hypomagnesemia affects roughly one-third of people with type 2 diabetes mellitus (T2DM) in pooled observational data and becomes more frequent in diabetic kidney disease (DKD). Reduced dietary intake accounts for part of the deficit; renal magnesium wasting linked to attenuated insulin signaling and reduced TRPM6 activity at the distal convoluted tubule is a plausible mechanism for the remainder, characterized mainly in cellular and experimental systems. In observational cohorts, lower serum magnesium accompanies poorer glycemic control and an excess of cardiovascular and microvascular events, and in DKD it independently predicts progression to kidney failure. Prescribed oral repletion has been associated with fewer cardiovascular events in hypomagnesemic patients, with no corresponding association in normomagnesemic ones, in propensity-matched data that cannot substitute for randomized confirmation. Mendelian randomization offers suggestive evidence for coronary artery disease and none for incident T2DM, a dissociation compatible with insulin resistance acting upstream of renal magnesium wasting, although instrument limitations leave other readings open. Hypomagnesemia is substantially less frequent in adult type 1 diabetes, where the association with glycemic control concentrates among patients with the highest insulin requirements. SGLT2 inhibitors raise serum magnesium modestly, whereas thiazide and loop diuretics and proton-pump inhibitors lower it. Randomized trials have shown modest effects on glycemic intermediates, larger in patients with documented deficiency, and no trial has yet tested renal progression. Magnesium status is a reproducible prognostic marker in T2DM and DKD; its value as a therapeutic target awaits randomized trials with clinical endpoints.
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BibTeX
@article{gembillo2026magnesium,
title = {{Magnesium in Diabetes Mellitus and Diabetic Kidney Disease}},
author = {Guido Gembillo and Luca Visconti and Luca Soraci and Lorenzo Lo Cicero and Manuel Scapellato and Concetto Sessa and Walter Morale and Antonino Catalano and Andrea Corsonello and Alberto La Spada and Ankit Sharma and Michele Provenzano and Domenico Santoro},
journal = {Journal of clinical medicine},
year = {2026},
month = oct,
doi = {10.3390/jcm15197723},
url = {https://europepmc.org/article/PMC/PMC13666300},
note = {CC BY},
}
RIS
TY - JOUR
TI - Magnesium in Diabetes Mellitus and Diabetic Kidney Disease
AU - Guido Gembillo
AU - Luca Visconti
AU - Luca Soraci
AU - Lorenzo Lo Cicero
AU - Manuel Scapellato
AU - Concetto Sessa
AU - Walter Morale
AU - Antonino Catalano
AU - Andrea Corsonello
AU - Alberto La Spada
AU - Ankit Sharma
AU - Michele Provenzano
AU - Domenico Santoro
PY - 2026
DA - 2026/10/01
JO - Journal of clinical medicine
DO - 10.3390/jcm15197723
UR - https://europepmc.org/article/PMC/PMC13666300
AB - Magnesium is a cofactor in cellular energy metabolism and insulin signaling, with recognized effects on vascular tone and cardiac electrophysiology. Hypomagnesemia affects roughly one-third of people with type 2 diabetes mellitus (T2DM) in pooled observational data and becomes more frequent in diabetic kidney disease (DKD). Reduced dietary intake accounts for part of the deficit; renal magnesium wasting linked to attenuated insulin signaling and reduced TRPM6 activity at the distal convoluted tubule is a plausible mechanism for the remainder, characterized mainly in cellular and experimental systems. In observational cohorts, lower serum magnesium accompanies poorer glycemic control and an excess of cardiovascular and microvascular events, and in DKD it independently predicts progression to kidney failure. Prescribed oral repletion has been associated with fewer cardiovascular events in hypomagnesemic patients, with no corresponding association in normomagnesemic ones, in propensity-matched data that cannot substitute for randomized confirmation. Mendelian randomization offers suggestive evidence for coronary artery disease and none for incident T2DM, a dissociation compatible with insulin resistance acting upstream of renal magnesium wasting, although instrument limitations leave other readings open. Hypomagnesemia is substantially less frequent in adult type 1 diabetes, where the association with glycemic control concentrates among patients with the highest insulin requirements. SGLT2 inhibitors raise serum magnesium modestly, whereas thiazide and loop diuretics and proton-pump inhibitors lower it. Randomized trials have shown modest effects on glycemic intermediates, larger in patients with documented deficiency, and no trial has yet tested renal progression. Magnesium status is a reproducible prognostic marker in T2DM and DKD; its value as a therapeutic target awaits randomized trials with clinical endpoints.
SN - 2077-0383
ER -