Semin Nephrol. 2026 Sep 29:151727. doi: 10.1016/j.semnephrol.2026.151727. Online ahead of print.
ABSTRACT
Hyperkalemia is a consequential complication of chronic kidney disease (CKD), and clinical guidance has traditionally restricted potassium-rich foods despite the potential benefits of plant-rich diets. This guidance also does not address potassium added during food processing, such as potassium chloride, phosphate, citrate, and lactate. This review examines potassium intake and clinical outcomes in CKD in the context of food additives, drawing on three indirect bodies of evidence: (1) dietary potassium intake and clinical outcomes, (2) potassium source and serum potassium response, and (3) trials of potassium-based salt substitutes. Measured potassium intake is more often associated with neutral or favorable outcomes than harm across mortality, cardiovascular events, and CKD progression, providing little support for blanket restriction of potassium-rich whole foods. Total dietary potassium is a poor predictor of serum potassium, whereas soluble potassium salts are more bioavailable and can more readily raise serum potassium, with cardiovascular benefit from salt substitution in low-risk populations but hyperkalemia risk in susceptible patients. These findings argue against treating dietary potassium as a uniform exposure in CKD, and potassium source, not total intake alone, should guide counseling. Direct evidence on additive-derived potassium and clinical outcomes remains needed to guide practice, research, and food policy.
PMID:42810931 | DOI:10.1016/j.semnephrol.2026.151727