Effects of Potassium or Sodium Supplementation on Mineral Homeostasis: A Controlled Dietary Intervention Study

Author:

Humalda Jelmer K1,Yeung Stanley M H1,Geleijnse Johanna M2ORCID,Gijsbers Lieke2,Riphagen Ineke J3,Hoorn Ewout J4,Rotmans Joris I5,Vogt Liffert6,Navis Gerjan1,Bakker Stephan J L1,de Borst Martin H1ORCID

Affiliation:

1. Department of Internal Medicine, Division of Nephrology, University of Groningen, University Medical Center Groningen, RB Groningen, the Netherlands

2. Division of Human Nutrition and Health, Wageningen University, HB Wageningen, the Netherlands

3. Department of Laboratory Medicine, University of Groningen, University Medical Center Groningen, RB Groningen, the Netherlands

4. Department of Internal Medicine, Division of Nephrology & Transplantation, Erasmus Medical Center, University Medical Center Rotterdam, CA Rotterdam, The Netherlands

5. Department of Internal Medicine, Leiden University Medical Center, RC Leiden, the Netherlands

6. Department of Internal Medicine, Section of Nephrology, Amsterdam Cardiovascular Sciences, Amsterdam University Medical Centers, University of Amsterdam, DD Amsterdam Zuidoost, the Netherlands

Abstract

Abstract Context Although dietary potassium and sodium intake may influence calcium-phosphate metabolism and bone health, the effects on bone mineral parameters, including fibroblast growth factor 23 (FGF23), are unclear. Objective Here, we investigated the effects of potassium or sodium supplementation on bone mineral parameters. Design, setting, participants We performed a post hoc analysis of a dietary controlled randomized, blinded, placebo-controlled crossover trial. Prehypertensive individuals not using antihypertensive medication (n = 36) received capsules containing potassium chloride (3 g/d), sodium chloride (3 g/d), or placebo. Linear mixed-effect models were used to estimate treatment effects. Results Potassium supplementation increased plasma phosphate (from 1.10 ± 0.19 to 1.15 ± 0.19 mmol/L, P = 0.004), in line with an increase in tubular maximum of phosphate reabsorption (from 0.93 ± 0.21 to 1.01 ± 0.20 mmol/L, P < 0.001). FGF23 decreased (114.3 [96.8-135.0] to 108.5 [93.5-125.9] RU/mL, P = 0.01), without change in parathyroid hormone and 25-hydroxy vitamin D3. Fractional calcium excretion decreased (from 1.25 ± 0.50 to 1.11 ± 0.46 %, P = 0.03) without change in plasma calcium. Sodium supplementation decreased both plasma phosphate (from 1.10 ± 0.19 to 1.06 ± 0.21 mmol/L, P = 0.03) and FGF23 (from 114.3 [96.8-135.0] to 108.7 [92.3-128.1] RU/mL, P = 0.02). Urinary and fractional calcium excretion increased (from 4.28 ± 1.91 to 5.45 ± 2.51 mmol/24 hours, P < 0.001, and from 1.25 ± 0.50 to 1.44 ± 0.54 %, P = 0.004, respectively). Conclusions Potassium supplementation led to a decrease in FGF23, which was accompanied by increase in plasma phosphate and decreased calcium excretion. Sodium supplementation reduced FGF23, but this was accompanied by decrease in phosphate and increase in fractional calcium excretion. Our results indicate distinct effects of potassium and sodium intake on bone mineral parameters, including FGF23. Clinical Trial Registration number NCT01575041

Funder

TI Food and Nutrition

Dutch Kidney Foundation

Publisher

The Endocrine Society

Subject

Biochemistry (medical),Clinical Biochemistry,Endocrinology,Biochemistry,Endocrinology, Diabetes and Metabolism

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