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In another trial, the effect of sodium restriction on BP and proteinuria was
investigated in CKD patients. The study involved 20 hypertensive stage 3–4 CKD
patients. Dietary education was individualized to the participant’s food prefer-
ences and was provided by an accredited practicing dietitian. A double-blind
placebo- controlled randomized crossover trial was performed to assess the effects
of high versus low sodium intake on ambulatory BP, 24-h protein and albumin
excretion, fluid status (body composition monitor), renin and aldosterone levels,
and arterial stiffness (pulse wave velocity and augmentation index) in 20 adult
patients with hypertensive stage 3–4 CKD as phase 1 of the LowSALT CKD
study. Ambulatory BP showed a mean reduction of 9.7/3.9 mm Hg (systolic BP/
diastolic BP) which was achieved from the high salt period to the low salt period.
Fluid volume, body weight, proteinuria, and albuminuria were also reduced in the
low salt period. Plasma renin and plasma aldosterone increased. This is the first
double-blind randomized controlled trial to assess the effect of sodium restriction
on ambulatory BP and other cardiovascular risk factors in non-dialyzed, non-
transplanted CKD patients. This study found that reducing dietary sodium intake
by 100 mmol reduced extracellular volume by 0.8 L with concurrent BP reduc-
tions of approximately 10/4 mm Hg SBP/DBP, a considerable magnitude of
change comparable with that expected from the addition of an antihypertensive
medication [ 47 ].
In the post hoc analysis of LowSALT CKD study, peripheral systolic BP was
reduced by mean 10 [95% CI 1–20] mm Hg from mean ±SD 159 ± 14 mm Hg at the
high sodium period to 148 ± 21 mm Hg at the low sodium period (p = 0.04), while
diastolic BP was reduced by 6 [95% CI 1–10] mm Hg from 87 ± 10 mm Hg at the
high sodium to 82 ± 12 mm Hg at the low sodium period (p = 0.03). Central systolic
BP was reduced by 13 [95% CI 2–24] mm Hg from 143 ± 20 mm Hg at the high
sodium period to 130 ± 21 mm Hg at the low sodium period (p = 0.03) Central pulse
pressure was significantly reduced by 9 [95% CI 2–17] mm Hg from 59 ± 16 mm
Hg at the high sodium period to 50 ± 12 mm Hg at the low sodium period (p = 0.02).
Fluid markers including extracellular/intracellular fluid ratio and NT–proBNP were
decreased in low sodium group compared to high sodium group [ 48 ].
In hemodialysis (HD) patients, sodium mass balance is primarily dependent on
dietary salt intake and sodium removal during dialysis. Thus simply reducing
sodium intake is the most logical approach to prevent hypervolemia. However, salt
restriction has not been performed in many dialysis centers [ 49 ] though the fact that
plasma sodium is closely related with BP in hemodialysis patients [ 50 , 51 ]. In
hypertensive peritoneal dialysis patients, total sodium load, daily total sodium
removal, extracellular water, and normalized extracellular water were all higher
compared to normotensive group [ 52 ].
Kayikcioglu et al. investigated the effect of salt restriction in HD patients. They
divided the patients into two groups. In first group (n: 190) salt restriction strategy
(5 g/day) was performed. In second group (n: 204) antihypertensive-based strategy
was applied. Salt restriction was defined as managing high BP via lowering dry
weight by strict salt restriction and insistent ultrafiltration without using antihyper-
tensive drugs. Antihypertensive drugs were used in 7% of the patients in first group
B. Afsar and A. Kirkpantur