Natriuretic response to an acute oral potassium load in healthy individuals and patients with chronic kidney disease: a randomized controlled trial.

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.