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Abstract: SA-PO0396

Serum Magnesium and Metabolic Phenotypes in CKD: Insights from the CRIC Study

Session Information

Category: Cardiovascular-Kidney-Metabolic Health

  • 602 Cardiovascular-Kidney-Metabolic Health: Clinical

Authors

  • Correa, Simon, Brigham and Women's Hospital, Boston, Massachusetts, United States
  • Mc Causland, Finnian R., Brigham and Women's Hospital, Boston, Massachusetts, United States
Background

Hypomagnesemia is common in chronic kidney disease (CKD) and linked to insulin resistance (IR), but use of the homeostatic model assessment (HOMA)-IR may be confounded by reduced insulin clearance in CKD. Whether serum magnesium (sMg) is associated with other metrics of metabolic disease requires further exploration.

Methods

We analyzed CRIC participants with non-missing baseline sMg and fasting metabolic labs. Exposure: baseline sMg (per 1 mg/dL lower). Outcomes: (1) log HOMA-IR; (2) triglyceride-glucose (TyG) index; (3) ATP-III metabolic syndrome (MetS) component score (0–5). Linear regression models were fit, adjusting for age, sex, race, BMI, diabetes, prior CVD, smoking, race-free CKD-EPI eGFR, log-24 hour proteinuria, statin, diuretic, and PPI use. Cubic splines were fit to explore non-linear associations.

Results

Among 5,266 participants (mean age 60 years, eGFR 47 mL/min/1.73m2, 51% diabetic), mean sMg was 1.9 ±0.3 mg/dL, median HOMA-IR was 4.1 [2.5, 7.3], mean TyG was 8.9 ±0.7, and mean MetS was 3.0 ±1.3. Lower sMg per 1mg/dL was associated with 14% higher HOMA-IR (95%CI 4, 26), 0.26 higher TyG (95%CI 0.19, 0.33), and 0.4 higher metabolic score (95%CI 0.3, 0.5). The association of serum magnesium with the metabolic score appeared to differ by baseline eGFR (P-interaction=0.02; Figure 1), but no differential associations were noted for HOMA-IR or TyG.

Conclusion

In a large CKD cohort, lower serum magnesium was independently associated with metrics of insulin resistance and broader metabolic dysfunction. Magnesium may serve as a modifiable marker linking mineral metabolism to insulin resistance, warranting further investigation as a therapeutic target in CKD.

Funding

  • NIDDK Support