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.