Cited by 34Potassium and Related DisordersIon Transport and Channel RegulationSodium Intake and Health

Kaliuresis in normal subjects following oral potassium citrate intake without increased plasma potassium concentration

Calò, L., Borsatti, A., Favaro, S., Rabinowitz, L.·2008·Nephron

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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Crossref · 10.1159/000188466

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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].”

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Authors
Calò, L., Borsatti, A., Favaro, S., & Rabinowitz, L.
Affiliations
  • University of Padua (IT)
  • University of California, Davis (US)
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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