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Cited by 26Parathyroid Disorders and TreatmentsSodium Intake and HealthBone health and osteoporosis research

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

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Humalda, Jelmer K, Yeung, Stanley M H, Geleijnse, Johanna M, Gijsbers, Lieke, Riphagen, Ineke J, Hoorn, Ewout J, Rotmans, Joris I, Vogt, Liffert, Navis, Gerjan, Bakker, Stephan J L, de Borst, Martin H·2020·The Journal of Clinical Endocrinology & Metabolism
DOI 10.1210/clinem/dgaa359PMC PMC7365698
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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

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Research works printed but not linked: 60

  1. Cordain, 2005, Origins and evolution of the Western diet: health implications for the 21st century, Am J Clin Nutr., 81, 341, 10.1093/ajcn.81.2.341 · DOI · Paper page
  2. Medina-Remón, 2018, Dietary patterns and the risk of obesity, type 2 diabetes mellitus, cardiovascular diseases, asthma, and neurodegenerative diseases, Crit Rev Food Sci Nutr., 58, 262, 10.1080/10408398.2016.1158690 · DOI
  3. Hariharan, 2015, The western diet and chronic kidney disease, Curr Hypertens Rep., 17, 16, 10.1007/s11906-014-0529-6 · DOI
  4. Movassagh, 2017, Current evidence on the association of dietary patterns and bone health: a scoping review, Adv Nutr., 8, 1, 10.3945/an.116.013326 · DOI
  5. Aburto, 2013, Effect of increased potassium intake on cardiovascular risk factors and disease: systematic review and meta-analyses, Bmj., 346, f1378, 10.1136/bmj.f1378 · DOI
  6. Eisenga, 2016, Urinary potassium excretion, renal ammoniagenesis, and risk of graft failure and mortality in renal transplant recipients, Am J Clin Nutr., 104, 1703, 10.3945/ajcn.116.134056 · DOI
  7. Mente, 2016, Associations of urinary sodium excretion with cardiovascular events in individuals with and without hypertension: a pooled analysis of data from four studies, Lancet., 388, 465, 10.1016/S0140-6736(16)30467-6 · DOI · Paper page
  8. Kestenbaum, 2005, Serum phosphate levels and mortality risk among people with chronic kidney disease, J Am Soc Nephrol., 16, 520, 10.1681/ASN.2004070602 · DOI
  9. Floege, 2011, Serum iPTH, calcium and phosphate, and the risk of mortality in a European haemodialysis population, Nephrol Dial Transplant., 26, 1948, 10.1093/ndt/gfq219 · DOI
  10. Yoo, 2016, Sex, age, and the association of serum phosphorus with all-cause mortality in adults with normal kidney function, Am J Kidney Dis., 67, 79, 10.1053/j.ajkd.2015.06.027 · DOI
  11. Souma, 2016, Fibroblast growth factor 23 and cause-specific mortality in the general population: The Northern Manhattan Study, J Clin Endocrinol Metab., 101, 3779, 10.1210/jc.2016-2215 · DOI
  12. Eisenga, 2019, Iron deficiency, elevated erythropoietin, fibroblast growth factor 23, and mortality in the general population of the Netherlands: a cohort study, Plos Med., 16, e1002818, 10.1371/journal.pmed.1002818 · DOI
  13. Vervloet, 2019, Renal and extrarenal effects of fibroblast growth factor 23, Nat Rev Nephrol., 15, 109, 10.1038/s41581-018-0087-2 · DOI
  14. Lips, 2006, Vitamin D physiology, Prog Biophys Mol Biol., 92, 4, 10.1016/j.pbiomolbio.2006.02.016 · DOI · Paper page
  15. Bienaimé, 2011, Vitamin D metabolism and activity in the parathyroid gland, Mol Cell Endocrinol., 347, 30, 10.1016/j.mce.2011.05.031 · DOI
  16. Shimada, 2004, FGF-23 is a potent regulator of vitamin D metabolism and phosphate homeostasis, J Bone Miner Res., 19, 429, 10.1359/JBMR.0301264 · DOI · Paper page
  17. Koizumi, 2013, Parathyroid function in chronic kidney disease: role of FGF23-Klotho axis, Contrib Nephrol., 180, 110, 10.1159/000346791 · DOI
  18. Blau, 2015, The PTH-Vitamin D-FGF23 axis, Rev Endocr Metab Disord., 16, 165, 10.1007/s11154-015-9318-z · DOI
  19. Jimbo, 2014, Fibroblast growth factor 23 accelerates phosphate-induced vascular calcification in the absence of Klotho deficiency, Kidney Int., 85, 1103, 10.1038/ki.2013.332 · DOI
  20. Silswal, 2014, FGF23 directly impairs endothelium-dependent vasorelaxation by increasing superoxide levels and reducing nitric oxide bioavailability, Am J Physiol Endocrinol Metab., 307, E426, 10.1152/ajpendo.00264.2014 · DOI
  21. Bouma-de Krijger, 2020, Fibroblast growth factor 23: are we ready to use it in clinical practice?, J Nephrol.
  22. Eckberg, 2015, Impact of westernization on fibroblast growth factor 23 levels among individuals of African ancestry, Nephrol Dial Transplant., 30, 630, 10.1093/ndt/gfu342 · DOI
  23. Frassetto, 2008, Adverse effects of sodium chloride on bone in the aging human population resulting from habitual consumption of typical American diets, J Nutr., 138, 419S, 10.1093/jn/138.2.419S · DOI
  24. Dawson-Hughes, 2015, Potassium bicarbonate supplementation lowers bone turnover and calcium excretion in older men and women: a randomized dose-finding trial, J Bone Miner Res., 30, 2103, 10.1002/jbmr.2554 · DOI
  25. Kong, 2017, Dietary potassium intake is beneficial to bone health in a low calcium intake population: the Korean National Health and Nutrition Examination Survey (KNHANES) (2008–2011), Osteoporos Int., 28, 1577, 10.1007/s00198-017-3908-4 · DOI
  26. Fatahi, 2018, The association of dietary and urinary sodium with bone mineral density and risk of osteoporosis: a systematic review and meta-analysis, J Am Coll Nutr., 37, 522, 10.1080/07315724.2018.1431161 · DOI
  27. Lin, 2003, The DASH diet and sodium reduction improve markers of bone turnover and calcium metabolism in adults, J Nutr., 133, 3130, 10.1093/jn/133.10.3130 · DOI
  28. Gijsbers, 2015, Effects of sodium and potassium supplementation on blood pressure and arterial stiffness: a fully controlled dietary intervention study, J Hum Hypertens., 29, 592, 10.1038/jhh.2015.3 · DOI
  29. 2019, NEVO-Tabel 2019.
  30. de Jong, 2019, Effects of dapagliflozin on circulating markers of phosphate homeostasis, Clin J Am Soc Nephrol., 14, 66, 10.2215/CJN.04530418 · DOI
  31. Blaine, 2015, Renal control of calcium, phosphate, and magnesium homeostasis, Clin J Am Soc Nephrol., 10, 1257, 10.2215/CJN.09750913 · DOI
  32. Kenny, 1973, Tests of phosphate reabsorption, Lancet., 2, 158, 10.1016/S0140-6736(73)93112-7 · DOI
  33. Riphagen, 2016, Effects of potassium supplementation on markers of osmoregulation and volume regulation, J Hypertens., 34, 215, 10.1097/HJH.0000000000000786 · DOI
  34. Jaeger, 1983, Influence of acute potassium loading on renal phosphate transport in the rat kidney, Am J Physiol., 245, F601
  35. Sebastian, 1990, Dietary potassium influences kidney maintenance of serum phosphorus concentration, Kidney Int., 37, 1341, 10.1038/ki.1990.120 · DOI
  36. Rubinacci, 2000, Bone as an ion exchange system: evidence for a pump-leak mechanism devoted to the maintenance of high bone K+, Am J Physiol Metab., 278, E15
  37. Gritter, 2018, Rationale and design of a randomized placebo-controlled clinical trial assessing the renoprotective effects of potassium supplementation in chronic kidney disease, Nephron., 140, 48, 10.1159/000490261 · DOI
  38. Wolf, 2012, Update on fibroblast growth factor 23 in chronic kidney disease, Kidney Int., 82, 737, 10.1038/ki.2012.176 · DOI
  39. Isakova, 2011, Fibroblast growth factor 23 and risks of mortality and end-stage renal disease in patients with chronic kidney disease, JAMA., 305, 2432, 10.1001/jama.2011.826 · DOI
  40. Marthi, 2018, Fibroblast growth factor-23 and risks of cardiovascular and noncardiovascular diseases: a meta-analysis, J Am Soc Nephrol., 29, 2015, 10.1681/ASN.2017121334 · DOI
  41. hr, 2018, FGF23 in cardiovascular disease: innocent bystander or active mediator?, Front Endocrinol (Lausanne)., 9
  42. Araki, 2015, Urinary potassium excretion and renal and cardiovascular complications in patients with type 2 diabetes and normal renal function, Clin J Am Soc Nephrol., 10, 2152, 10.2215/CJN.00980115 · DOI
  43. Filippini, 2017, The effect of potassium supplementation on blood pressure in hypertensive subjects: a systematic review and meta-analysis, Int J Cardiol., 230, 127, 10.1016/j.ijcard.2016.12.048 · DOI
  44. Lemann, 1991, Potassium administration reduces and potassium deprivation increases urinary calcium excretion in healthy adults [corrected], Kidney Int., 39, 973, 10.1038/ki.1991.123 · DOI
  45. Moseley, 2013, Potassium citrate supplementation results in sustained improvement in calcium balance in older men and women, J Bone Miner Res., 28, 497, 10.1002/jbmr.1764 · DOI
  46. He, 2010, Effects of potassium chloride and potassium bicarbonate on endothelial function, cardiovascular risk factors, and bone turnover in mild hypertensives, Hypertension., 55, 681, 10.1161/HYPERTENSIONAHA.109.147488 · DOI
  47. Frassetto, 2000, Comparative effects of potassium chloride and bicarbonate on thiazide-induced reduction in urinary calcium excretion, Kidney Int., 58, 748, 10.1046/j.1523-1755.2000.00221.x · DOI
  48. van der Wijst, 2018, Effects of a high-sodium/low-potassium diet on renal calcium, magnesium, and phosphate handling, Am J Physiol Renal Physiol., 315, F110, 10.1152/ajprenal.00379.2017 · DOI
  49. Andrukhova, 2014, FGF23 promotes renal calcium reabsorption through the TRPV5 channel, Embo J., 33, 229
  50. Asplin, 2006, Urine calcium excretion predicts bone loss in idiopathic hypercalciuria, Kidney Int., 70, 1463, 10.1038/sj.ki.5001778 · DOI
  51. Jovanovich, 2013, Fibroblast growth factor 23, bone mineral density, and risk of hip fracture among older adults: the cardiovascular health study, J Clin Endocrinol Metab., 98, 3323, 10.1210/jc.2013-1152 · DOI
  52. Rupp, 2019, High FGF23 levels are associated with impaired trabecular bone microarchitecture in patients with osteoporosis, Osteoporos Int., 30, 1655, 10.1007/s00198-019-04996-7 · DOI
  53. Humalda, 2016, Response of fibroblast growth factor 23 to volume interventions in arterial hypertension and diabetic nephropathy, Medicine (Baltimore)., 95, e5003, 10.1097/MD.0000000000005003 · DOI
  54. Hu, 2018, Effect of salt intervention on serum levels of fibroblast growth factor 23 (FGF23) in Chinese adults: an intervention study, Med Sci Monit., 24, 1948, 10.12659/MSM.906489 · DOI · Paper page
  55. Steele, 1970, Increased urinary phosphate excretion following volume expansion in normal man, Metabolism., 19, 129, 10.1016/S0026-0495(70)90210-6 · DOI
  56. Andrukhova, 2014, FGF23 regulates renal sodium handling and blood pressure, EMBO Mol Med., 6, 744, 10.1002/emmm.201303716 · DOI
  57. van Ballegooijen, 2016, Renal clearance of mineral metabolism biomarkers, J Am Soc Nephrol., 27, 392, 10.1681/ASN.2014121253 · DOI
  58. Damasio, 2011, The role of salt abuse on risk for hypercalciuria, Nutr J., 10, 3, 10.1186/1475-2891-10-3 · DOI
  59. Coe, 2016, Idiopathic hypercalciuria and formation of calcium renal stones, Nat Rev Nephrol., 12, 519, 10.1038/nrneph.2016.101 · DOI
  60. Robertson, 2016, Dietary recommendations and treatment of patients with recurrent idiopathic calcium stone disease, Urolithiasis., 44, 9, 10.1007/s00240-015-0849-2 · DOI

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Metadata

Authors
Humalda, J. K., Yeung, S. M. H., Geleijnse, J. M., Gijsbers, L., Riphagen, I. J., Hoorn, E. J., Rotmans, J. I., Vogt, L., Navis, G., Bakker, S. J. L., & de Borst, M. H.
Affiliations
  • University Medical Center Groningen (NL)
  • Wageningen University & Research (NL)
  • Erasmus MC (NL)
  • Leiden University Medical Center (NL)
  • Amsterdam University Medical Centers (NL)
Corresponding author
de Borst, Martin H
ORCID
Venue
The Journal of Clinical Endocrinology & Metabolism
Publisher
The Endocrine Society
Published
2020-06-07
Volume
105
Issue
9
Pages
e3246-e3256
ISSN
  • 0021-972X (ISSN-L)
  • 1945-7197
DOI
10.1210/clinem/dgaa359
PMC
PMC7365698
OpenAlex
W3033353847
Cited by
26
References
5
Citations by year
2026: 6 · 2025: 1 · 2024: 6 · 2023: 5 · 2022: 4 · 2021: 4
FWCI
2.04
Type
journal article
Language
en
Open access
Licence
Locations
  • The Journal of Clinical Endocrinology & Metabolism (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • EUR Research Repository (Erasmus University Rotterdam) (publishedVersion, other-oa)
  • University of Groningen research database (University of Groningen / Centre for Information Technology) (publishedVersion, cc-by)
  • Socio-Environmental Systems Modeling (acceptedVersion, cc-by)
  • Leiden Repository (Leiden University) (submittedVersion, cc-by)
  • Pure Amsterdam UMC (submittedVersion, cc-by)
  • Data Archiving and Networked Services (DANS) (submittedVersion, other-oa)
  • EUR Research Repository (Erasmus University Rotterdam) (submittedVersion, other-oa)
  • RePub (Erasmus University Rotterdam) (submittedVersion, other-oa)
  • Data Archiving and Networked Services (DANS) (submittedVersion, cc-by)
  • University of Groningen research database (University of Groningen / Centre for Information Technology) (submittedVersion, cc-by)
Funders
  • TI Food and Nutrition (CH001)
  • Dutch Kidney Foundation (CP1601)
Topics
  • Health Sciences › Medicine › Nephrology › Parathyroid Disorders and Treatments
  • Health Sciences › Nursing › Nutrition and Dietetics › Sodium Intake and Health
  • Health Sciences › Medicine › Orthopedics and Sports Medicine › Bone health and osteoporosis research
Keywords
potassium supplementation, sodium supplementation, mineral homeostasis, fibroblast growth factor 23, plasma phosphate, renal phosphate reabsorption, prehypertension, dietary salt, calcium and phosphorus metabolism, parathyroid hormone, vitamin D3, urinary calcium excretion, bone health, dietary intervention, crossover trial
MeSH terms
Fibroblast Growth Factor-23, Aged, Aged, 80 and over, Bone and Bones, Calcium, Cholecalciferol, Double-Blind Method, Female, Homeostasis, Humans, Male, Middle Aged, Minerals, Parathyroid Hormone, Phosphates, Potassium, Retrospective Studies, Sodium, Dietary, Cross-Over Studies, Dietary Supplements, Prehypertension

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