Abstract: TH-PO140
Serum Magnesium and Progression of Coronary Artery Calcification: A Report from the Chronic Renal Insufficiency Cohort (CRIC) Study
Session Information
- CKD-MBD: Clinical
October 24, 2024 | Location: Exhibit Hall, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Bone and Mineral Metabolism
- 502 Bone and Mineral Metabolism: Clinical
Authors
- Mehmood, Mehreen, University Hospitals, Cleveland, Ohio, United States
- Kanthety, Radhika, University Hospitals, Cleveland, Ohio, United States
- Chen, Zhengyi, Case Western Reserve University, Cleveland, Ohio, United States
- Rahman, Mahboob, University Hospitals, Cleveland, Ohio, United States
- Dobre, Mirela A., University Hospitals, Cleveland, Ohio, United States
- Negrea, Lavinia Aura, University Hospitals, Cleveland, Ohio, United States
Background
Magnesium may play a protective role against the progression of vascular calcification in chronic kidney disease (CKD), however the evidence remains scarce. Higher serum magnesium levels are consistently associated with a reduced volume of vascular calcification in CKD populations. This study aims to evaluate the association between serum magnesium level and progression of coronary artery calcification (CAC) in a cohort of individuals with CKD enrolled in the Chronic Renal Insufficiency Cohort (CRIC) study. We hypothesize that low serum magnesium level, is a risk factor for CAC progression.
Methods
Serum magnesium and CAC were measured in 862 CRIC participants at baseline and after 3 years. CAC was measured using electron beam or multidetector computed tomography and calculated using Agatston score. CAC progression was defined as follows: CAC> 0 at follow-up if CAC=0 at baseline; annualized change ≥10 Agatston units at follow-up if 0<CAC≤100 at baseline; and annualized percent change (annualized change in CAC score divided by the baseline CAC score) ≥ 10% at follow-up, if CAC > 100 at baseline. Logistic regression models were built to study the association of interest.
Results
The mean eGFR was 44±15ml/min per 1.73m2, mean serum magnesium was 1.96± 0.28 mg/dL, and 42.7% participants had diabetes. A total of 412 (48%) participants experienced CAC progression. No significant correlation was observed between baseline magnesium level and total Agaston score (r=0.032, p=0.58). Compared to participants with high baseline magnesium level, those with low magnesium (<2 mg/dL) were more likely to have CAC >400 at baseline (59.3% vs 40.7%) but the difference was not statistically significant (p=0.62). Each mg/dL increase in magnesium level was associated with 17% lower but not statistically significant lower risk of CAC progression, in models adjusted for demographics, baseline co-morbidities, medications, calcium level, eGFR and proteinuria (OR 0.73; 95%CI: 0.32–1.64). Subgroup analyses by sex, race and CKD stages reveal similar findings.
Conclusion
In a cohort of patients with CKD stages 2-4, serum magnesium level was not associated with CAC progression. Further studies will be needed to test the magnesium's potential role to inhibit vascular calcification.