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Randomized Trial on the Effect of Oral Potassium Chloride Supplementation on the Thiazide-Sensitive Sodium Chloride Cotransporter in Healthy Adults

Publikation: Bidrag til tidsskrift/Konferencebidrag i tidsskrift /Bidrag til avis › Tidsskriftartikel › Forskning › peer review

DOI

  • Aihua Wu, University of Queensland
    • ,
  • Martin J. Wolley, University of Queensland, Royal Brisbane and Women's Hospital
    • ,
  • Hannah L. Mayr, University of Queensland, Princess Alexandra Hospital Brisbane, Metro South Hospital and Health Service
    • ,
  • Lei Cheng
  • Diane Cowley, University of Queensland
    • ,
  • Bo Li, University of Queensland
    • ,
  • Katrina L. Campbell, University of Queensland
    • ,
  • Andrew S. Terker, Vanderbilt University
    • ,
  • David H. Ellison, Oregon Health & Science University
    • ,
  • Paul A. Welling, Johns Hopkins University
    • ,
  • Robert A. Fenton
  • Michael Stowasser, University of Queensland

Introduction: The putative “renal-K switch” mechanism links dietary potassium intake with sodium retention and involves activation of the sodium chloride (NaCl) cotransporter (NCC) in the distal convoluted tubule in response to low potassium intake, and suppression in response to high potassium intake. This study examined NCC abundance and phosphorylation (phosphorylated NCC [pNCC]) in urinary extracellular vesicles (uEVs) isolated from healthy adults on a high sodium diet to determine tubular responses to alteration in potassium chloride (KCl) intake. Methods: Healthy adults maintained on a high sodium (∼4.5 g [200 mmol]/d) low potassium (∼2.3 g [60 mmol]/d) diet underwent a 5-day run-in period followed by a crossover study, with 5-day supplementary KCl (active phase, Span-K 3 tablets (potassium 24 mmol) thrice daily) or 5-day placebo administrated in random order and separated by 2-day washout. Ambulatory blood pressure (BP) and biochemistries were assessed, and uEVs were analyzed by western blotting. Results: Among the 18 participants who met analysis criteria, supplementary KCl administration (vs. placebo) was associated with markedly higher levels of plasma potassium and 24-hour urine excretion of potassium, chloride, and aldosterone. KCl supplementation was associated with lower uEV levels of NCC (median fold change (KCl/Placebo) = 0.74 [0.30–1.69], P < 0.01) and pNCC (fold change (KCl/Placebo) = 0.81 [0.19–1.75], P < 0.05). Plasma potassium inversely correlated with uEV NCC (R2 = 0.11, P = 0.05). Conclusions: The lower NCC and pNCC in uEVs in response to oral KCl supplementation provide evidence to support the hypothesis of a functional “renal-K switch” in healthy human subjects.

OriginalsprogEngelsk
TidsskriftKidney international reports
Vol/bind8
Nummer6
Sider (fra-til)1201-1212
Antal sider12
ISSN2468-0249
DOI
StatusUdgivet - jun. 2023

Bibliografisk note

Funding Information:
This work is supported by a grant from the Leducq Foundation (17CVD05, Potassium in Hypertension Network). AW was supported by a scholarship from the Commonwealth Government of Australia. RAF was funded by the Novo Nordisk Foundation ( NNF21OC0067647 , NNF17OC0029724 )

Publisher Copyright:
© 2023 International Society of Nephrology

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