What question did this study set out to answer?

This study aims to assess how different potassium salts affect serum T50 values, particularly in healthy and CKD patients.

June 3, 2026

Effect of an Acute Potassium Load on Serum T50 in Healthy Subjects and Patients With Chronic Kidney Disease

Key Points

This study aims to assess how different potassium salts affect serum T50 values, particularly in healthy and CKD patients.
Randomized trial involving 18 healthy controls and 9 CKD stage G3b-G4 patients
Participants received oral potassium chloride or potassium citrate, or placebo, with prior lisinopril pretreatment
T50 was measured at baseline, 1 h, 2 h, and 4 h using linear mixed models
T50 increased significantly after potassium citrate but not after potassium chloride or placebo
Plasma potassium levels increased more in CKD patients, enhanced by lisinopril, regardless of potassium type
Baseline T50 values were similar for healthy controls (375 ±34 min) and CKD (389 ±35 min; p=0.19)

Abstract

Objective: Chronic kidney disease (CKD) is associated with accelerated vascular calcification and increased cardiovascular risk. Low T50 values indicate higher calcification propensity, which triggers vascular calcification, leading to increased pulse wave velocity and associated adverse cardiovascular outcomes. Since dietary potassium has been associated with lower cardiovascular risk and plasma potassium influence mineral metabolism, this study evaluated the effect of two different potassium salts with and without RAAS blockade on serum T50 in healthy subjects and CKD patients. Design and method: Healthy controls (HC) and non-diabetic CKD stage G3b-G4 patients received a single oral load of 40 mmol potassium chloride (KCl), 40 mmol potassium citrate (K-cit), or placebo in random order with and without 6-week lisinopril pretreatment. T50-analyses were run on serum obtained at baseline and after 1 h, 2 h and 4 h. Linear mixed models with age, sex, calcium, phosphate and T50 values at baseline as covariates, were used to assess between and within-group differences. Results: We included 18 HC (mean age 28, 61% male) and 9 CKD patients (mean age 62, 78% male). At baseline, both plasma potassium and calcium concentrations were similar between the groups, but phosphate levels differed (HC: 1.06 ±0.2 mmol/L; CKD: 0.93 ±0.2 mmol/L; p<0.001). Baseline T50 values were similar for HC (375 ±34 min) and CKD patients (389 ±35 min) (p=0.19). Higher age and phosphate levels were associated with lower baseline T50, but not plasma potassium. Plasma potassium increase upon supplementation was higher in CKD than HC—an effect that was augmented by lisinopril and did not depend on the type of potassium supplement. T50 increased significantly after K-cit, but not after placebo and KCl—showing a similar peak increase at 2 h in both groups. Lisinopril pretreatment did not influence the T50 increase upon potassium supplementation. Conclusions: Potassium citrate significantly prolonged T50 values in both healthy participants and CKD patients in a similar magnitude, whereas potassium chloride did not. Our findings suggest that the alkalizing component of potassium citrate, rather than potassium itself may protect against vascular calcification both in CKD and non-renal patients

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