Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2026
Natriuretic response to an acute oral potassium load in healthy individuals and patients with chronic kidney disease: a randomized controlled trial.
СтатьяРандомизированное исследованиеНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Wouda Rosa D, Karsten Micky, Michels Erik H A, Garrelds Ingrid M, Danser A H Jan, de Borst Martin H, Hoorn Ewout J, Rotmans Joris I, Vogt Liffert
Аннотация
BACKGROUND: The health benefits of dietary potassium have been linked to potassium-induced natriuresis. However, it is unknown whether potassium loading in patients with chronic kidney disease (CKD) induces natriuresis and to what degree it increases plasma potassium. We hypothesize that potassium-induced natriuresis remains intact and that potassium loading is safe in patients with CKD.
METHODS: In this placebo-controlled crossover study, 18 healthy individuals and 9 patients with non-diabetic CKD stage G3b-G4 received an acute oral load of potassium chloride (KCl), potassium citrate (K-cit) (40 mmol each) or placebo, either with or without 6 weeks of lisinopril (10 mg/day) pretreatment. Differences in placebo-subtracted plasma potassium and natriuresis between groups during 4-h follow-up were analysed using linear mixed models.
RESULTS: In healthy individuals, but not in patients with CKD, urinary sodium excretion increased 2 h after potassium supplementation, independent of lisinopril pretreatment. Compared with patients with CKD, mean urinary sodium excretion in healthy individuals was 13 mmol [95% confidence interval (CI) 4-22; P = .005] and 13 mmol (95% CI 4-22; P = .006) higher 2 h after KCl and K-cit, respectively. Estimated glomerular filtration rate positively correlated with urinary sodium excretion 2 h after KCl and K-cit, both with and without lisinopril pretreatment. Plasma potassium after potassium supplementation was higher in patients with CKD than in healthy individuals independent of lisinopril pretreatment.
CONCLUSIONS: These findings indicate that in CKD, potassium-induced natriuresis does not occur and oral potassium loading is accompanied by an increased risk of hyperkalaemia.
METHODS: In this placebo-controlled crossover study, 18 healthy individuals and 9 patients with non-diabetic CKD stage G3b-G4 received an acute oral load of potassium chloride (KCl), potassium citrate (K-cit) (40 mmol each) or placebo, either with or without 6 weeks of lisinopril (10 mg/day) pretreatment. Differences in placebo-subtracted plasma potassium and natriuresis between groups during 4-h follow-up were analysed using linear mixed models.
RESULTS: In healthy individuals, but not in patients with CKD, urinary sodium excretion increased 2 h after potassium supplementation, independent of lisinopril pretreatment. Compared with patients with CKD, mean urinary sodium excretion in healthy individuals was 13 mmol [95% confidence interval (CI) 4-22; P = .005] and 13 mmol (95% CI 4-22; P = .006) higher 2 h after KCl and K-cit, respectively. Estimated glomerular filtration rate positively correlated with urinary sodium excretion 2 h after KCl and K-cit, both with and without lisinopril pretreatment. Plasma potassium after potassium supplementation was higher in patients with CKD than in healthy individuals independent of lisinopril pretreatment.
CONCLUSIONS: These findings indicate that in CKD, potassium-induced natriuresis does not occur and oral potassium loading is accompanied by an increased risk of hyperkalaemia.