Oral KCl Supplementation Safely Reduces Body Na⁺ Surplus and Blood Pressure

Potassium-enriched table salt lowers blood pressure (BP) and reduces cardiovascular mortality. Whether these beneficial effects stem from reduced Na⁺ intake, increased K⁺ intake, or both is unknown. We tested the hypothesis that oral potassium chloride (KCl) supplementation lowers body Na⁺ content and BP in patients with essential hypertension (EH) or hyperaldosteronism, independent of salt intake.

Between February 2024 and February 2025, we conducted a single-arm, prospective, longitudinal study with nonrandomized oral KCl intervention in 40 participants with hypertension. All received personalized (blood K⁺-adjusted) KCl supplementation (Span-K tablets) for 6 to 9 weeks. After the intervention, participants completed a routine diagnostic workup and were classified with EH or hyperaldosteronism. Primary end point: baseline muscle Na⁺ surplus in hyperaldosteronism. Secondary end point: interventional muscle Na⁺ mobilization and BP reduction.

Seventeen participants were diagnosed with EH, and 23 with hyperaldosteronism. At baseline, patients with hyperaldosteronism showed higher muscle Na⁺ content (24.67±2.93 versus 22.48±3.37 mmol/L tissue volume, P=0.023; primary end point). Oral KCl increased 24-hour urine K⁺ excretion without altering 24-hour urine Na⁺. KCl supplementation successfully eliminated the muscle Na⁺ surplus in the hyperaldosteronism group (-1.90 mmol/L tissue volume [CI, -3.20 to -0.60]; P=0.005; secondary end point), lowered blood Na⁺/K⁺ ratios in both groups (EH, -5.34 [CI, -7.69 to -2.99]; P=4.6×10^-5; hyperaldosteronism, -7.02 [CI, -9.04 to -5.01]; P=2.1×10^-8), and reduced systolic BP (EH, -8.33 mm Hg [CI, -14.55 to -2.12]; P=0.010; hyperaldosteronism, -7.35 mm Hg [CI, -12.69 to -2.01]; P=0.008). To account for early study termination, a conservative significance threshold of α=0.025 was implemented, which all end points crossed.

Oral KCl supplementation mobilizes intracellular Na⁺ stores, corrects pathological Na⁺/K⁺ distribution, and lowers BP across hypertension phenotypes. This safe, targeted approach warrants consideration as a scalable public health strategy for cardiovascular disease prevention.

URL: https://www.clinicaltrials.gov; Unique identifier: NCT06569589.