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Low serum magnesium is associated with faster decline in kidney function: the Dallas Heart Study experience
  1. Silvia Ferrè1,2,
  2. Xilong Li3,
  3. Beverley Adams-Huet1,3,
  4. Naim M Maalouf1,2,
  5. Khashayar Sakhaee1,2,
  6. Robert D Toto3,4,
  7. Orson W Moe1,4,5,
  8. Javier A Neyra1,2,6
  1. 1Charles and Jane Pak Center for Mineral Metabolism and Clinical Research, UT Southwestern Medical Center, Dallas, TX, USA
  2. 2Department of Internal Medicine, Division of Mineral Metabolism, UT Southwestern Medical Center, Dallas, TX, USA
  3. 3Department of Clinical Sciences, Division of Biostatistics, UT Southwestern Medical Center, Dallas, TX, USA
  4. 4Department of Internal Medicine, Division of Nephrology, UT Southwestern Medical Center, Dallas, TX, USA
  5. 5Department of Physiology, UT Southwestern Medical Center, Dallas, TX, USA
  6. 6Department of Internal Medicine, Division of Nephrology, Bone and Mineral Metabolism, University of Kentucky, Lexington, KY, USA
  1. Correspondence to Dr Silvia Ferrè, Department of Internal Medicine, UT Southwestern Medical Center, Dallas TX 75390, USA; silvia.ferre{at}utsouthwestern.edu and Dr Javier A Neyra, Department of Internal Medicine, Division of Nephrology, Bone, and Mineral Metabolism, University of Kentucky, 800 Rose St, MN668, Lexington, KY, 40536, USA; javier.neyra{at}uky.edu

Abstract

Hypomagnesemia associates with inflammation and risk of diabetes and hypertension, which may contribute to kidney function decline. We hypothesized that low serum magnesium (SMg) levels independently associate with a significant decline in estimated glomerular filtration rate (eGFR). We analyzed SMg levels in 2056 participants from the Dallas Heart Study, a longitudinal, population‐based, multiethnic, cohort study involving residents of Dallas County, Texas, USA. The primary study outcome was the change in eGFR using multivariable linear regression models adjusted for demographics, anthropometric and biochemical parameters, medications, C reactive protein levels, prevalent hypertension and diabetes. During a median follow-up of 7.0 years (25th, 75th percentile: 6.5, 7.6), the median decrease in eGFR was −0.71 (25th, 75th percentile: −2.43, +0.68) mL/min/1.73 m2 per year in the entire cohort. In a fully adjusted model, the lowest SMg quintile (≤1.9 mg/dL or ≤0.8 mM) was associated with a −0.50 mL/min/1.73 m2 per year drop in eGFR (95% CI −0.95 to –0.05; p=0.028) compared with the highest SMg quintile (≥2.3 mg/dL or ≥1.0 mM). Every 0.2 mg/dL (0.08 mM) decrease in SMg was associated with an eGFR decline of −0.23 mL/min/1.73 m2 per year (95% CI −0.38 to –0.08; p=0.003), a decline that was more pronounced in participants with prevalent diabetes compared with patients without diabetes (−0.51 vs −0.18 mL/min/1.73 m2 per year, respectively). In conclusion, low SMg was independently associated with eGFR decline. Further studies are needed to determine whether Mg repletion can ameliorate inflammation, lower blood pressure and serum glucose and ultimately prevent or retard kidney function decline.

  • magnesium
  • hypomagnesemia
  • chronic kidney disease
  • diabetes mellitus
  • hypertension

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Footnotes

  • Contributors Study concept and design: SF and JN. Acquisition, analysis or interpretation of data: SF, XL, BAH and JN. Drafting of the manuscript: SF and JN. Critical revision of the manuscript for intellectual content: NMM, KS, RT and OM. Statistical analysis: SF, XL, BAH and JN. Obtained funding: RT and OM. Study supervision: NMM, KS, RT, OM and JN.

  • Funding The Dallas Heart Study is supported by grant UL1TR001105 from the National Center for Advancing Translational Science of the National Institutes of Health. This work was also supported by the University of Texas Southwestern Medical Center O’Brien Kidney Research Center (P30-DK079328). Dr Ferrè was supported by the Charles and Jane Pak Center Innovative Research Support Award. Dr Neyra is currently supported by an Early Career Pilot Grant from the National Center for Advancing Translational Sciences, National Institutes of Health, through Grant UL1TR001998.

  • Competing interests None declared.

  • Ethics approval The UT Southwestern Institutional Review Board approved the study.

  • Provenance and peer review Not commissioned; externally peer reviewed.

  • Patient consent for publication Obtained.

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