Kaliuresis in normal subjects following oral potassium citrate intake without increased plasma potassium concentration
Abstract
Ingestion of potassium salts typically induces both a kaliuresis and an increase in the systemic plasma potassium concentration. In this study normal healthy adults undergoing water diuresis ingested potassium citrate or sodium citrate (0.5 mmol/kg body weight) or continued without ion ingestion (a time control group). Urine was collected over 20-min intervals and venous blood sampled at midinterval. Intake of potassium citrate led to a significant increase in potassium excretion that began during the first postingestion collection and peaked 60-80 min after intake with a maximal increase in potassium excretion above baseline of 1.60 mumol/min.kg-1. The kaliuresis occurred without changes in plasma potassium concentration, excretion of creatinine or calcium, or urine hypo-osmolality and was associated with a briefer, smaller, and less regular increase in sodium excretion and a pronounced but irregular increase in chloride excretion. Plasma aldosterone was insignificantly elevated above baseline, and the initial increase did not occur until 40-60 min after potassium intake. Intake of sodium citrate did not produce a kaliuresis. The cause of the kaliuresis does not appear to be an increased systemic plasma potassium concentration, an increased plasma level of aldosterone, intake of citrate, or an elevated excretion of sodium. The mechanism inducing the kaliuresis following oral potassium intake in the absence of changes in systemic plasma potassium may involve a reflex initiated at potassium sensors in gut, portal vein, or liver.
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K+ intake activates a feedforward control in which distal tubule K+ secretion is stimulated before changes in plasma K+ concentration or aldosterone concentration can be observed.
“K+ intake has been shown to activate a feedforward control in which distal tubule K+ secretion is stimulated before changes in plasma K+ concentration or ALD concentration can be observed [1, 15–18].”
From A mathematical model of potassium homeostasis: Effect of feedforward and feedback controls (2022) · cites this paper as [15]
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ResultA mathematical model of potassium homeostasis: Effect of feedforward and feedback controls
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Mir, S., Özkayın, N., & Ertan, P. (2003)
- Authors
- Calò, L., Borsatti, A., Favaro, S., & Rabinowitz, L.
- Affiliations
- University of Padua (IT)
- University of California, Davis (US)
- ORCID
- Calò, L.
- Venue
- Nephron
- Publisher
- S. Karger AG
- Published
- 2008-12-17
- Volume
- 69
- Issue
- 3
- Pages
- 253-258
- ISSN
- 1660-8151 (ISSN-L)
- 2235-3186
- OpenAlex
- W2024434444
- Cited by
- 33
- References
- 0
- Citations by year
- 2026: 1 · 2025: 2 · 2023: 2 · 2022: 3 · 2020: 2 · 2016: 2 · 2015: 3 · 2014: 1 · 2013: 3 · 2012: 1
- FWCI
- 1.53
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- The Nephron journals/Nephron journals (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Potassium and Related Disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion Transport and Channel Regulation
- Health Sciences › Nursing › Nutrition and Dietetics › Sodium Intake and Health
- Keywords
- potassium excretion, potassium citrate, sodium citrate, plasma potassium, aldosterone, sodium excretion, chloride excretion, citrate, potassium sensing, water diuresis
- MeSH terms
- Administration, Oral, Adult, Citrates, Diuresis, Female, Homeostasis, Humans, Male, Potassium, Water, Citric Acid
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