Natriuretic Response to an Acute Oral Potassium Load in Healthy Individuals and Patients with Chronic Kidney Disease: A Randomized Controlled Trial

Abstract Background and Hypothesis 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 which 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/d) pretreatment. Differences in placebo-subtracted plasma potassium and natriuresis between groups during 4-h follow-up were analyzed using linear mixed models. Results In healthy individuals, but not in patients with CKD, urinary sodium excretion increased 2 hours after potassium supplementation, independent of lisinopril pretreatment. Compared to patients with CKD, urinary sodium excretion (mean [95% CI]) in healthy individuals was 13 [4, 22] mmol (p = 0.005) and 13 [4, 22] mmol (p = 0.006) higher 2 hours after KCl and K-cit, respectively. eGFR positively correlated with urinary sodium excretion 2 hours 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 hyperkalemia.