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Abstract: TH-PO211

Association Between Serum Magnesium and Arterial Calcification in Incident Hemodialysis Patients

Session Information

Category: Bone and Mineral Metabolism

  • 402 Bone and Mineral Metabolism: Clinical

Authors

  • Chen, Wei, University of Rochester School of Medicine, Rochester, New York, United States
  • Fitzpatrick, Jessica, The Hospital For Sick Children , Toronto, Ontario, Canada
  • Monroy-Trujillo, Jose Manuel, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States
  • Sozio, Stephen M., Johns Hopkins University School of Medicine, Baltimore, Maryland, United States
  • Jaar, Bernard G., Johns Hopkins University School of Medicine, Baltimore, Maryland, United States
  • Estrella, Michelle M., University of California, San Francisco and San Francisco VA Medical Center, San Francisco, California, United States
  • Wu, Tong tong, University of Rochester School of Medicine, Rochester, New York, United States
  • Melamed, Michal L., Albert Einstein College of Medicine, Bronx, New York, United States
  • Parekh, Rulan S., The Hospital For Sick Children , Toronto, Ontario, Canada
  • Bushinsky, David A., University of Rochester School of Medicine, Rochester, New York, United States

Group or Team Name

  • PACE study team
Background

Animal studies demonstrate that magnesium (Mg) supplementation inhibits arterial calcification in CKD. In humans, both CKD and diabetes mellitus (DM) are independent risk factors for arterial calcification; however, it is unknown if Mg influences calcification in CKD patients and whether DM alters this potential relationship. We tested the hypotheses that higher serum Mg concentration was associated with lower coronary artery calcification (CAC) and thoracic aortic calcification (TAC) scores in incident hemodialysis (HD) patients and that these associations, if any, were modified by DM.

Methods

We performed cross-sectional analyses of 367 incident HD patients in the Predictors of Arrhythmic and Cardiovascular Risk in ESRD (PACE) cohort. Serum Mg was measured on a non-HD day. CAC and TAC were quantified with computed tomography, which was done at a median time of 3.6 months after initiation of HD. We used logistic regression to study the association of Mg with CAC (>0 vs. 0) and TAC (>0 vs. 0) scores among all participants and linear regression for log-transformed CAC among those with CAC >0. Models were tested for interaction with DM status and adjusted for age, sex, race, smoking, body mass index, serum calcium, phosphate, parathyroid hormone, albumin, hemoglobin, low-density lipoprotein and Kt/V.

Results

Mean age was 55 years; 40% were female; 72% were black and 58% had DM. Mean serum Mg was 1.8±0.2 mEq/L; 63% had CAC >0 and 50% had TAC >0. DM did not modify the association between Mg and CAC. Among all participants, Mg was not associated with CAC. However, among those with CAC >0, per 0.1 mEq/L higher Mg, CAC score was 15% lower [% change: -15% (95% CI: -25%, -3%), p=0.02]. DM modified the association between Mg and TAC (p for interaction=0.003). Per 0.1 mEq/L higher serum Mg, the odds of having TAC >0 was 34% lower [OR: 0.66 (95% CI: 0.47, 0.92), p=0.02] among non-diabetics, but was 55% greater [OR: 1.55 (95% CI 1.08, 2.23), p=0.02] among diabetics.

Conclusion

Consistent with animal studies, higher serum Mg was associated with a lower CAC score among incident HD patients with CAC >0 and with a lower odds of having TAC >0 among non-diabetics. Why Mg was associated with a higher odds of having TAC >0 among diabetics remains to be elucidated.

Funding

  • NIDDK Support