Introduction:
Patients with chronic kidney disease (CKD) are at an increased risk of CVD compared to the general population. Left ventricular hypertrophy (LVH) is an independent risk factor for CVD in the general population and in CKD patients. In the general population, sodium (Na) excretion is directly associated with LVH. However, this association has not been examined in patients with CKD.
Hypothesis:
We hypothesized that in CKD patients, urinary Na excretion would be directly and urinary potassium (K) would be indirectly associated with development of ejection fraction (EF) < 50% and LVH and longitudinal changes in EF and left ventricular mass index (LVMI).
Methods:
The Chronic Renal Insufficiency Cohort Study (CRIC) is a prospective cohort study of 3,939 participants with CKD. Dietary Na and K excretion were assessed by averaging three 24-hour urinary measures (over 2 years) and calibrated to sex-specific mean 24-hour urinary creatinine excretion. Echocardiograms (ECHO) were conducted at follow-up years 1, 4, and 7 and centrally analyzed to quantify EF and LVMI. LVH is defined as LVMI ≥ 47 g/m
2.7
in women and LVMI ≥ 50 g/m
2.7
in men. Log-linear binomial and linear mixed effects models were used.
Results:
During follow-up, 676 participants developed EF <50% and 238 developed LVH among those with EF ≥ 50% or free of LVH at the first ECHO, respectively. After multivariate adjustment, participants in the highest quartile of adjusted sodium excretion (>196.2 mmol/24 hours) had a relative risk of 1.31 (95% CI 1.08, 1.59) of developing an EF < 50% during follow-up compared to those in the lowest quartile (<127.8 mmol/24 hours). Furthermore, participants in the highest quartile of adjusted urinary sodium excretion had a greater annual decrease in ejection fraction (-1.36%, 95 CI: -1.53, -1.19%) compared to those in the lowest quartile (-0.95%, 95% CI: -1.11, -0.79%; p for trend across quartiles 0.0003). No significant association was observed between K excretion and development of EF < 50% or change in EF. In addition, no association was observed between adjusted Na or K excretion and development of LVH or change in LVMI during follow-up.
Conclusions:
Higher Na excretion is associated with a greater likelihood of developing an EF <50% and a greater annual decrease in EF. Further studies are needed to determine if interventions to reduce high dietary sodium could slow the decline in left ventricular structure and function in patients with CKD.
Association of N-Terminal Pro-B-Type Natriuretic Peptide With Left Ventricular Structure and Function in Chronic Kidney Disease (from the Chronic Renal Insufficiency Cohort [CRIC])
