ReviewJournal of clinical medicine2026
Magnesium in Diabetes Mellitus and Diabetic Kidney Disease.
Review in Journal of clinical medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
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.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.