ORIGINAL ARTICLE Dietary salt intake is related to inflammation and albuminuria in primary hypertensive patients R Yilmaz, H Akoglu, B Altun, T Yildirim, M Arici and Y Erdem 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 ¼ 76, mean urine sodium: 111.7 ± 29.1 mmol/24 h), medium- salt-intake group (n ¼ 77, mean urine sodium: 166.1 ± 16.3 mmol/24 h) and high-salt-intake group (n ¼ 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 ¼ 0.0003 and P ¼ 0.001, respectively). CRP was positively correlated with 24-h urinary sodium excretion (r ¼ 0.28, P ¼ 0.0008) and albuminuria, whereas albuminuria was positively correlated with 24-h urinary sodium excretion (r ¼ 0.21, P ¼ 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. European Journal of Clinical Nutrition (2012) 66, 1214–1218; doi:10.1038/ejcn.2012.110; published online 22 August 2012 Keywords: albuminuria; hypertension; inflammation; salt intake INTRODUCTION Salt intake is an important factor in the genesis of primary hypertension. Epidemiological and clinical data have showed that high salt intake is associated with increased risk of cardiovascular diseases and stroke. 1 Recent work has provided further evidence that high dietary salt intake may even partly cause blood pressure (BP) -independent target organ damage including left ventricular hypertrophy and microalbuminuria. 2–4 Microalbuminuria is a significant predictor of endothelial dysfunction and an indepen- dent marker of cardiovascular diseases in patients with primary hypertension. 5,6 Several studies have demonstrated that high salt intake is positively related to urinary albumin excretion and this relation may be independent of BP. 3,4,7 The mechanisms responsible for this effect are unclear. In animal models, dietary salt overload has been demonstrated to contribute to renal injury documented by albuminuria and decreased glomerular filtration rate with a minimally increased arterial pressure. 8,9 Inflammatory mechanisms have been proposed to have a role in this nephrotoxic effect of salt excess. 9–13 The role of inflammation in the initiation and progression of cardiovascular diseases is increasingly recognized. 14,15 Studies in hypertensive individuals have shown increased plasma and vascular tissue levels of C-reactive protein (CRP) and several inflammatory cytokines, suggesting a potential association between vascular inflammation and hypertension. 16–19 Although the evidence for a direct relationship between salt intake and BP is basically established, 20–23 the clinical evidence is not adequate to consider whether this effect translates into increased incidence of cardiovascular diseases independent from BP in patients with high dietary salt consumption. In this study, we hypothesized that dietary salt intake may be related with inflammation and albuminuria independently from BP in non-diabetic hypertensive patients. MATERIALS AND METHODS Study population A total of 289 patients who had been previously diagnosed as primary hypertension and who were under anti-hypertensive treatment at least 3 months were recruited from patients presenting to our outpatient nephrology clinic for follow-up treatment of primary hypertension within a period of 12 months. From the 289 patients, we excluded 65 patients meeting at least one of the following criteria: patients with diabetes mellitus or coronary heart disease (n ¼ 26), chronic inflammatory diseases (n ¼ 3), glomerular filtration rate o60 ml/min/1.73 m 2 (n ¼ 12), urine albumin greater than 300 mg/day (n ¼ 10) and patients on diuretic therapy (n ¼ 14). Therefore, 224 non-diabetic hypertensive patients were enrolled in this study. Demographic findings of all patients including age, gender, smoking status, number and class of anti-hypertensive drugs currently used were recorded. All patients underwent BP and anthropometric measurements (height in cm, body weight in kg), and venous blood drawing. Twenty-four hour urine was collected from all participants for measurement of sodium and albumin excretion. To verify a correct urine sampling, 24-h urinary creatinine excretion was measured. Office BP was measured using a mercury sphygmomanometer after at least 15 min of rest in the sitting position. Patients were asked to remove all clothing that covers the location of cuff and were comfortably seated, with the legs uncrossed and Department of Nephrology, Hacettepe University Faculty of Medicine, Ankara, Turkey. Correspondence: Dr R Yilmaz, Department of Nephrology, Hacettepe University Faculty of Medicine, Sihhiye, Ankara 06100, Turkey. E-mail: drrahmiy@hotmail.com Received 20 April 2012; revised 24 July 2012; accepted 25 July 2012; published online 22 August 2012 European Journal of Clinical Nutrition (2012) 66, 1214–1218 & 2012 Macmillan Publishers Limited All rights reserved 0954-3007/12 www.nature.com/ejcn