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Kidney Week

Abstract: PO0557

Potassium Supplementation Decreases Plasma Fibroblast Growth Factor 23 and Increases Plasma Phosphate in Stage 3b-4 CKD Patients: Single-Arm Intervention Study

Session Information

Category: Bone and Mineral Metabolism

  • 402 Bone and Mineral Metabolism: Clinical


  • Yeung, Stanley M.H., Universitair Medisch Centrum Groningen, Groningen, Groningen, Netherlands
  • Gritter, Martin, Erasmus MC, Rotterdam, Zuid-Holland, Netherlands
  • Wouda, Rosa D., Amsterdam UMC Locatie AMC, Amsterdam, North Holland, Netherlands
  • Bakker, Stephan J.L., Universitair Medisch Centrum Groningen, Groningen, Groningen, Netherlands
  • Van Zanden, Jelmer J., Martini Ziekenhuis, Groningen, Groningen, Netherlands
  • Rotmans, Joris I., Leids Universitair Medisch Centrum, Leiden, Zuid-Holland, Netherlands
  • Hoorn, Ewout J., Erasmus MC, Rotterdam, Zuid-Holland, Netherlands
  • Vogt, Liffert, Amsterdam UMC Locatie AMC, Amsterdam, North Holland, Netherlands
  • De Borst, Martin H., Universitair Medisch Centrum Groningen, Groningen, Groningen, Netherlands

Advanced chronic kidney disease (CKD) is characterized by mineral and bone disorders (MBD) including elevated fibroblast growth factor 23 (FGF23). Recent studies in healthy subjects showed that potassium supplementation decreases FGF23. Here, we investigated whether potassium supplementation reduces FGF23 and other MBD parameters in patients with CKD.


We performed a post-hoc analysis of a 2-week open-label run-in phase from a clinical trial in patients with CKD stage G3b-G4 (NCT03253172). Patients received potassium chloride (KCl, 40 mmol/day). Baseline and post-treatment blood and urine samples were collected. Mixed model analyses were used to assess effects of potassium supplementation on MBD parameters.


We included 135 patients in whom KCl supplementation increased plasma phosphate (from 1.0±0.2 to 1.1±0.2 mmol/L, P=0.001) and tubular phosphate reabsorption (from 0.64±0.20 to 0.69±0.20 mmol/L, P<0.001). KCl supplementation, when adjusted for estimated glomerular filtration rate, decreased C-terminal FGF23 (cFGF23) (from 140.5 [Interquartile range [IQR] 105.9–217.4] to 131.5 [IQR 105.8–212.8] RU/mL, P=0.03), intact FGF23 (from 69.6 [IQR 46.6–107.1] to 62.9 [IQR 41.7–104.6] pg/mL, P=0.003) and vitamin D (72.5 [IQR 43.9–92.9] to 70.2 [IQR 44.2–90.1] nmol/L, P<0.001). Parathyroid hormone, plasma calcium, 24hrs urinary calcium excretion, α-Klotho, and IL-6 did not change.
At baseline, 37 participants were vitamin D deficient (<50 nmol/L). The decrease in cFGF23 by KCl supplementation depended on baseline vitamin D status (P-interaction=0.02), and was present in vitamin D sufficient (147.2 [IQR 108.3–216.8] to 130.9 [IQR 105.5–218.0] RU/mL, P=0.03), while it was not in vitamin D deficient patients (131.5 [IQR 104.0–230.7] to 133.0 [IQR 106.8–211.0] RU/mL, P=0.32).


In this short-term interventional study, KCl supplementation reduced FGF23 and coincided with increased plasma phosphate levels and vitamin D. Reduction in cFGF23 by KCl was only present in vitamin D sufficient patients. Dietary potassium intake might decrease FGF23 levels and vitamin D status should be sufficient before FGF23 lowering strategies could be applied in patients with CKD.