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

BACKGROUND: 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. METHODS: 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. RESULTS: 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. CONCLUSIONS: 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. REGISTRATION: URL: https://www.clinicaltrials.gov ; Unique identifier: NCT06569589.