26524-h UNa (salt 1 g/day) for BP > 130/80 mm Hg was 1.26 (95% CI 1.10–1.44,
P = 0.001). The sodium restriction group achieved significantly more reduction in
systolic BP (−11.1 mm Hg vs. −5.0 mmHg, P = 0.022), diastolic BP (−9.4 mm Hg
vs. −2.1 mmHg, P = 0.009), and urine protein excretion [−465 (−855 to −340) mg/
day vs. −150 (−570 to 40) mg/day, P = 0.024]. A positive correlation was observed
between the change of 24-h UNa and the change of SBP (r = 0.450, P = 0.047) in
the sodium restriction group. The change of 24-h UNa was also correlated with the
24-h TGF-β1 excretion (r = 0.558, P = 0.011) in these patient. The authors recom-
mended that dietary sodium intake restriction should be monitored and intensified
in the treatment of Chinese CKD patients [ 42 ].
In one recent observational study, Meng et al. investigated the relationship
between salt intake and BPs in non-dialysis CKD patients. To determine salt intake,
patients were given written instructions on how to collect the 24-h urine under nor-
mal eating habits. A urine aliquot (100 ml) from the 24-h urine collection was
assayed. BP/dietary sodium intake was regarded as salt sensitivity index. The
authors demonstrated that there was a linear positive relationship between the salt
intake and the SBP but there was no relationship between salt intake and
DBP. According to CKD stages, there was no correlation between the salt intake
and the SBP in stage 1–2, but there was a linear regression relationship in stage 3, 4
and strongest in stage 5 [ 43 ].
Regarding the effect of salt intake on resistant HT, there is even scarce data. In
an evaluation of subjects with severe hypertension (but not specifically mentioned
as resistant HT), Fotherby et al. assessed the BP effects of low dietary salt ingestion
in 17 untreated hypertensive subjects with a mean office BP of 176 ± 17 and
96 ± 11 mm Hg. After 5 weeks of low-salt diet (80–100 mmol/24 h), 24-h systolic
and diastolic BP decreased by 5 and 2 mm Hg [ 44 ].
In a study by Gavras et al., a greater BP reduction was observed with extreme
dietary salt restriction in combination with intense diuretic therapy in subjects with
uncontrolled BP on maximal doses of at least two agents (a diuretic and a sympa-
tholytic agent). In this study, BP decreased on average by 21/7 mm Hg during inges-
tion of a diet limited to 10 mmol of sodium with concurrent administration of either
hydrochlorothiazide 100 mg or furosemide 80–200 mg daily. However, again there
was no specific mention on RHT in this study [ 45 ].
The direct evidence between salt intake and RHT was shown in at least one clini-
cal study. Pimenta et al. examined the effects of dietary salt restriction on office and
24-h ambulatory blood pressure in 12 subjects with resistant hypertension on an aver-
age of 3.4 ± 0.5 antihypertensive medications and a mean office BP of
145.8 ± 10.8/83.9 ± 11.2 mm Hg. Patients entered into a randomized crossover evalu-
ation of low (50 mmol/24 h × 7 days) and high sodium diets (250 mmol/24 h × 7
days) separated by a 2-week washout period. The mean urinary sodium excretion was
46.1 ± 26.8 versus 252.2 ± 64.6 mmol/24 h during low-salt versus high-salt intake. A
low-salt compared with a high-salt diet decreased office systolic and diastolic BPs by
22.7 and 9.1 mm Hg, respectively. This was the first study, to assess the effects of low
dietary salt ingestion in subjects with resistant hypertension. However, in this study
patients with creatinine clearance <60 mL/min were excluded from the study [ 46 ].
16 Treatment of Hypertension in Light of the New Guidelines: Salt Intake