Dietary salt intake is related to inflammation and albuminuria in primary hypertensive patients.

BACKGROUND/
OBJECTIVES: In this study, we hypothesized that dietary salt intake may be related with inflammation and albuminuria independently from blood pressure (BP) in non-diabetic hypertensive patients. SUBJECTS/
METHODS: A total of 224 patients with primary hypertension were included in the study. Serum C-reactive protein (CRP) levels, 24-h urine sodium and albumin excretion were measured in all patients. The subjects were divided into tertiles according to the level of 24-h urinary sodium excretion: low-salt-intake group (n = 76, mean urine sodium: 111.7 ± 29.1 mmol/24 h), medium-salt-intake group (n = 77, mean urine sodium: 166.1 ± 16.3 mmol/24 h) and high-salt-intake group (n = 71, mean urine sodium: 263.6 ± 68.3 mmol/24 h).
RESULTS: Systolic and diastolic BP measurements of patients were similar in the three salt-intake groups. CRP and urinary albumin levels were significantly higher in high-salt-intake group compared with medium- and low-salt-intake groups (P = 0.0003 and P = 0.001, respectively). CRP was positively correlated with 24-h urinary sodium excretion (r = 0.28, P = 0.0008) and albuminuria, whereas albuminuria was positively correlated with 24-h urinary sodium excretion (r = 0.21, P = 0.0002). Multiple regression analysis revealed that urinary sodium excretion was an independent predictor of both CRP and albuminuria.
CONCLUSIONS: These findings suggest that high salt intake is associated with enhanced inflammation and target organ damage reflected by increased albuminuria in treated hypertensive patients independent of any BP effect.