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 D 3. 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.