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Abstract: PO2525

The Effect of Magnesium Supplementation on Vascular Calcification in CKD: A Randomised Clinical Trial (MAGiCAL-CKD)

Session Information

Category: Bone and Mineral Metabolism

  • 402 Bone and Mineral Metabolism: Clinical


  • Bressendorff, Iain Oshoj, Nordsjaellands Hospital, Hillerød, Denmark
  • Hansen, Ditte, Herlev Hospital, Herlev, Denmark
  • Schou, Morten, Herlev Hospital, Herlev, Denmark
  • Kragelund, Charlotte, Nordsjaellands Hospital, Hillerod, Denmark
  • Svensson, My, Akershus Universitetssykehus HF, Lorenskog, Norway
  • Hashemi, Bahram, Aalborg Universitetshospital, Aalborg, North Denmark Region, Denmark
  • Kristensen, Tilde, Hospitalsenhed Midt, Viborg, Denmark
  • Vrist, Marie Houmaa, Hospitalsenheden Vest, Holstebro, Denmark
  • Borg, Rikke, Sjaellands Universitetshospital Roskilde, Roskilde, Sjaelland, Denmark
  • Tougaard, Birgitte Godskesen, Sygehus Lillebalt Kolding Sygehus, Kolding, Denmark
  • Borg, Kristine, Odense Universitetshospital, Odense, Syddanmark, Denmark
  • Hjortkjær, Henrik Øder, Rigshospitalet, Kobenhavn, Denmark
  • Kristiansen, Cathrine Helgestad, Akershus Universitetssykehus HF, Lorenskog, Norway
  • Nasiri, Mohammad, Sydvestjysk Sygehus, Esbjerg, Syddanmark, Denmark
  • Ashraf, Haseem, Akershus Universitetssykehus HF, Lorenskog, Norway
  • Pasch, Andreas, Calciscon AG, Nidau, Switzerland
  • Brandi, Lisbet, Nordsjaellands Hospital, Hillerød, Denmark

Higher levels of serum magnesium (Mg) are associated with lower risk of cardiovascular (CV) events in patients with CKD and Mg prevents vascular calcification (VC) in animal models of CKD. We hypothesized that oral Mg supplementation would slow the progression of VC in CKD.


In a randomised, double-blind, placebo-controlled, parallel group, clinical trial we recruited 148 patients with an eGFR between 15 and 45 mL/min and randomised them to oral Mg hydroxide 15 mmol twice daily or matching placebo for 12 months. We excluded kidney transplant recipients. The primary endpoint was the between-groups difference in coronary artery calcification (CAC) score after 12 months adjusted for baseline CAC score (ANCOVA).


Seventy-five subjects were randomised to Mg and 73 to placebo. Median eGFR was 25 mL/min at baseline. Mg treatment significantly increased plasma Mg (p < 0.001). CAC scores were not significantly different between the two groups after 12 months (mean difference 0.01%, 95% CI –13.5% to 15.6%; p = 0.991). A prespecified subgroup analysis of subjects with CAC > 0 at baseline did not significantly alter the main results (mean difference 4.0%, 95% CI –5.4% to 14.3%).
Thirty-two subjects randomised to Mg treatment experienced gastrointestinal side effects compared to 11 subjects randomised to placebo. There were five deaths and six CV events in the Mg group, compared to two deaths and no CV events in the placebo group.


Mg supplementation did not slow the progression of VC in CKD, despite a significant increase in plasma Mg. There were more deaths and CV events in the Mg group compared to placebo, although the trial was not powered to investigate these endpoints.


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