Food and health

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



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.


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).


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.


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.


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, 3, 4 Microalbuminuria is a significant predictor of endothelial dysfunction and an independent 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, 10, 11, 12, 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, 17, 18, 19

Although the evidence for a direct relationship between salt intake and BP is basically established,20, 21, 22, 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=26), chronic inflammatory diseases (n=3), glomerular filtration rate <60 ml/min/1.73 m2 (n=12), urine albumin greater than 300 mg/day (n=10) and patients on diuretic therapy (n=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 the back and arm supported, such that the middle of the cuff on the upper arm was at the level of the right atrium. Cuff width was selected according to subject’s arm circumference. The cuff was inflated to at least 30 mm Hg above the point at which the radial pulse disappeared. The mercury column was deflated at 2–3 mm/s, and the first and last audible sounds were taken as systolic and diastolic BP. A minimum of two readings were taken at intervals of at least 1 min, and the average of these readings were used to represent the patient’s BP. If there was >5 mm Hg difference between the first and second readings, additional one or two readings were obtained, and then the average of these multiple readings was considered for the analysis. Venous blood samples were obtained after an overnight fast for the estimation of fasting glucose, lipid levels (total cholesterol, LDL-cholesterol, HDL-cholesterol and triglycerides), albumin, blood urea nitrogen, creatinine, complete blood count, erythrocyte sedimentation rate and CRP. Serum lipids were determined by using an autoanalyzer (Hitachi P800, Holliston, MA, USA). CRP was detected by rate nephelometry (IMMAGE Immunochemistry System, Beckerman Coulter, Inc., Fullerton, CA, USA). The CRP detection range corresponded to concentrations of 0.01–9.6 mg/dl (normal values <0.8 mg/dl). Urinary albumin was measured by immunonephelometry (Dade Behring Diagnostics, Marburg, Germany) with a lower limit of detection of 2.3 mg/l. The intra- and interassay CVs were 2.7% and 4.5%, respectively. Other biochemical variables were analyzed using standard laboratory techniques for hospital use.

At the end of the measurements, the subjects were divided into tertiles according to the level of 24-h urinary sodium excretion: low-salt-intake group (n=76, mean urinary sodium excretion: 111.7±29.1 mmol/24 h), medium-salt-intake group (n=77, mean urinary sodium excretion: 166.1±16.3 mmol/24 h) and high-salt-intake group (n=71, mean urinary sodium excretion: 263.6±68.3 mmol/24 h). The study protocol was approved by ethics committee of Hacettepe University, an institutional ethics committee. Informed consent was taken from all the participants.

Statistical analysis

Distribution of the variables was checked using the Kolmogorov–Smirnov test. Continuous variables with normal distribution were presented as mean±s.d. Variables with unequal distribution were expressed as median and interquartile ranges (Q1–Q3). Categorical variables were presented as numbers and percentages. To determine the presence of any difference between groups, if data were normally distributed and variances were homogeneous, one-way ANOVA was used, otherwise analyses were done with Kruskal–Wallis test. To determine the groups between which there was a statistically significant difference, Tukey’s HSD test was used, if the parametric test conditions were satisfied, and Mann–Whitney U test was used after Bonferoni correction, if the parametric test conditions were not satisfied. Categorical variables were compared with χ2 or Fischer’s exact test. Spearman’s correlation coefficients was calculated to evaluate the relationship between continous variables. Linear regression analysis was introduced so as to determine the independent associations of CRP and albuminuria. Statistical significance was considered at a two-tailed value of P<0.05. Statistical analyses were performed using SPSS software (Statistical Package for the Social Sciences, version 13.0; SPSS Inc., Chicago, IL, USA).


Demographic and biochemical characteristics of patients

Clinical and biochemical characteristics of the patients are shown in the Table 1. No differences were observed in terms of gender distribution, age, body mass index (BMI), smoking status, duration of hypertension, types of anti-hypertensive agents and laboratory findings between the low-, medium- and high-salt-intake groups.

Table 1 Demographic and biochemical characteristics of low-, medium- and high-salt-intake groupsa

Blood pressure measurements

Systolic and diastolic BP values of patients were similar despite the increasing levels of 24-h urinary sodium excretion in the study groups. To investigate whether the dose of anti-hypertensive therapy was a factor for similar BP values in the tertile groups, we also determined the number and types of anti-hypertensive drugs in the groups. Although the types of the drugs were similar between the groups, the mean number of anti-hypertensive drugs was significantly higher in high-salt-intake group compared with low- or medium-salt-intake groups (P=0.003 and P=0.009, respectively). However, the mean number of anti-hypertensive drugs did not differ between low- and medium-salt-intake groups (P=0.73; Table 1). To evaluate a possible association of 24-h urinary sodium excretion with BP measurements and number of anti-hypertensive drugs, we used bivariate correlation analysis. There were no significant correlations between 24-h urinary sodium excretion and systolic or diastolic BP (P=0.16 and P=0.47, respectively) in the whole study population, whereas 24-h urinary sodium excretion significantly correlated with the number of anti-hypertensive drugs (r=0.17, P=0.008).

Serum CRP and urinary albumin levels

Figure 1 shows CRP values as an inflammatory marker in low-, medium- and high-salt-intake groups. CRP was significantly higher in high-salt-intake group compared with medium- and low-salt-intake groups (P=0.0003). However, CRP levels did not differ between the low- and medium-salt-intake groups. Similarly, urinary albumin levels were higher in high-salt-intake group compared with medium- and low-salt-intake groups (P=0.001), whereas comparison of medium- and low-salt-intake groups revealed no difference (Figure 2). In correlation analysis, serum CRP levels were positively correlated with systolic BP (r=0.24, P=0.031), 24-h urinary sodium excretion (r=0.28, P=0.0008) and 24-h urinary albumin excretion (r=0.43, P=0.0001) in the whole study population. In a multiple regression analysis model, using CRP as the dependent variable, urinary sodium excretion and albuminuria were independent predictors of CRP (β=0.28, P=0.004 and β=0.46, P=0.0005, respectively; Table 2). In the total study population, the main correlates of urinary albumin excretion were 24-h urinary sodium excretion (r=0.21, P=0.0002), BMI (r=0.38, P=0.02) and serum creatinine level (r=0.16, P=0.005). A multiple regression analysis revealed that 24-h urinary sodium excretion and serum creatinine levels were independent predictors of albuminuria (β=0.22, P=0.0001 and β=0.17, P=0.003, respectively; Table 3). However, age, gender, smoking status, BMI, systolic and diastolic BP, and lipid levels did not correlate with albuminuria.

Figure 1

Median and distribution of serum CRP levels in low-, medium- and high-salt-intake groups. The bar in each box indicates the median value. Upper and lower borders of the boxes are the 25th and 75th percentiles, respectively. Maximum and minimum values are shown by the error bars (*P=0.0003).

Figure 2

Median and distribution of urinary albumin levels in low-, medium- and high-salt-intake groups. The bar in each box indicates the median value. Upper and lower borders of the boxes are the 25th and 75th percentiles, respectively. Maximum and minimum values are shown by the error bars (*P=0.001).

Table 2 Correlation analysis of c-reactive protein with different variables (a) and multivariable linear regression analysis showing independent variables associated with serum c-reactive protein as the dependent variable in treated hypertensive patients (b)
Table 3 Correlation analysis of urinary albumin with different variables (a) and multivariable linear regression analysis showing independent variables associated with urinary albumin as the dependent variable in treated hypertensive patients (b)


During the past decade, significant amount of data have indicated that high salt intake causes increased BP due to hypervolemia in short term and increased peripheral vascular resistance through the process of autoregulation in long term.24, 25 However, a clear relationship is not fully established, as the BP response to high salt intake is variable among individuals.23 In the present study, although the BP levels did not differ between the groups with the increasing amount of salt intake from low- to high-salt-intake groups, we observed that the patients in the high-salt-intake group required more antihypertensive drugs than the low- and medium-salt-intake groups to maintain the similar BP levels. Furthermore, we demonstrated a significant correlation between daily salt intake and number of anti-hypertensive agents required for the treatment. Therefore, our findings may indirectly confirm the results of studies that propose high salt intake causes high BP, at least by pointing out the association between dietary salt intake and intensity of anti-hypertensive therapy. Interestingly, although patients with high salt intake attained BP levels similar to those in low- and medium-salt-intake groups, serum CRP levels and albuminuria were significantly increased in high-salt-intake group. Additionally, 24-h urinary sodium excretion was significantly correlated with serum CRP levels and albuminuria. These findings suggest that under similar BP conditions, high salt intake is associated with inflammation and renal injury reflected by increased albuminuria.

To our knowledge, this is the first study that specifically showed a relation between salt intake and CRP in a treated hypertensive population. A number of cross-sectional studies demonstrated higher levels of CRP in treated or untreated patients with primary hypertension compared with normotensive individuals.17, 26, 27 However, greater plasma CRP concentrations among patients with hypertension might be explained by a clustering of common positive CRP covariates such as age, female sex, increased BMI and lipid concentrations.28, 29 In our study, we found urinary sodium excretion as an independent predictor of CRP, which suggests that high salt intake may be a novel covariate factor for high CRP levels in this population.

We also demonstrated that high salt intake was significantly associated with albuminuria independent of BP in treated hypertensive patients. This finding is consistent with the results of du Cailar et al.7 that documented a significant association between urinary sodium excretion and albuminuria despite similar values of systolic arterial pressure in a group of normotensive subjects and patients with untreated hypertension. In a review of available published information, Jones-Burton et al.30 also suggested that variations in dietary salt consumption directly influence albuminuria, with increasing salt intake associated with worsening albuminuria. Studies on animal models have proposed a link between dietary salt intake and target organ damage including ventricular hypertrophy and albuminuria. In these studies, high salt intake was found to be associated with increased collagen deposition and marked interstitial fibrosis in the left ventricle, glomeruli, renal tubules and in intramyocardial arteries and arterioles.31 High dietary salt intake also produced arterial injury without increasing BP.32 These effects of high salt intake on target organs are linked to the fibrogenic activity of transforming growth factor (TGF)-β1, as TGF-β1 production has been demonstrated to increase during high salt intake.33, 34 Indeed, the overexpression of TGF-β1 mRNA was demonstrated in the left ventricle and kidneys after a high-salt diet in animal studies.31

The present study demonstrated a positive correlation between albuminuria and serum CRP levels in treated hypertensive patients. CRP, a marker of systemic low-grade inflammation, and albuminuria are frequently elevated in essential hypertension and predict cardiovascular prognosis independent of conventional risk factors.35 The relation between CRP and albuminuria in untreated hypertensive patients has been demonstrated in several reports.35, 36, 37, 38 The underlying pathophysiological mechanisms for the observed relation between albuminuria and inflammatory processes in the setting of essential hypertension have not been well defined. However, it has been proposed that low-grade inflammation seen in hypertensive subjects may increase the likelihood of increased glomerular leakage of albumin in response to BP.35, 39 This glomerular leakage may involve either increased transmission of systemic BP or decreased barrier function of the glomerulus due to inflammatory involvement.38, 39, 40 In our study, regarding the near-normal BP levels of the patients under treatment in three salt-intake groups, serum CRP and urinary albumin levels were still higher in patients with high dietary salt intake. Furthermore, under the similar BP levels, urinary sodium excretion was correlated with both albuminuria and CRP. These findings suggest that increased glomerular leakage of albumin may reflect inflammation-mediated renal vascular injury rather than a response to elevated BP levels in our patient population. High dietary salt intake may contribute to this process directly via arterial injury or indirectly by augmenting the effects of inflammation.

However, the cross-sectional nature of our study limits the ability to conclude any causal relationship between salt intake, CRP levels and albuminuria. Moreover, CRP measurement was determined only once and we analyzed office BP measurements as ambulatory or home BP monitoring data of patients were not available. Given that these measurements may show intra-individual fluctuations, the accuracy of our results might be attenuated.

We did not find a correlation between albuminuria and age, gender, smoking, BMI, BP and lipid levels in this study. This may be related with hypertension treatment. Patients were prescribed many types of antihypertensive agents including ACE inhibitors, ARB, calcium channel blockers, beta-blockers and others. Effects of these drugs on albuminuria independent of BP-reducing effect may change the correlation analysis. In addition, sample size of the study and distribution characteristics of age, BMI, BP and lipid levels may also affect the results.

In conclusion, the major finding of the present study was that treated hypertensive patients with high dietary salt intake showed increased CRP concentrations and albuminuria. The relation of high salt intake with increased CRP and urinary albumin levels appeared independent of BP. These findings may suggest that under the similar BP conditions, high salt intake may be associated with enhanced inflammation and target organ damage reflected by increased albuminuria. Therefore, patients with high dietary salt intake may be at greater cardiovascular risk even though they are on appropriate anti-hypertensive medication. However, future, large and prospective studies are needed to confirm the relation between salt intake, inflammation and cardiovascular diseases.


  1. 1

    Tuomilehto J, Jousilahti P, Rastenyte D, Moltchanov V, Tanskanen A, Pietinen P et al. Urinary sodium excretion and cardiovascular mortality in Finland: a prospective study. Lancet 2001; 357: 848–851.

    CAS  Article  Google Scholar 

  2. 2

    Ritz E, Dikow R, Morath C, Schwenger V . Salt—a potential ‘uremic toxin’? Blood Purif 2006; 24: 63–66.

    CAS  Article  Google Scholar 

  3. 3

    Messerli FH, Schmieder RE, Weir MR . Salt. A perpetrator of hypertensive target organ disease? Arch Intern Med 1997; 157: 2449–2452.

    CAS  Article  Google Scholar 

  4. 4

    Verhave JC, Hillege HL, Burgerhof JG, Janssen WM, Gansevoort RT, Navis GJ et al. PREVEND Study Group. Sodium intake affects urinary albumin excretion especially in overweight subjects. J Intern Med 2004; 256: 324–330.

    CAS  Article  Google Scholar 

  5. 5

    Gerstein HC, Mann JF, Yi Q, Zinman B, Dinneen SF, Hoogwerf B et al. HOPE Study Investigators. Albuminuria and risk of cardiovascular events and heart failure in diabetic and nondiabetic individuals. JAMA 2001; 286: 421–426.

    CAS  Article  Google Scholar 

  6. 6

    Pedrinelli R, Dell’ Omo G, Di Bello V, Pontremolli R, Microalbuminuria Mariani M . an integrated marker of cardiovascular risk in essential hypertension. J Hum Hypertens 2002; 16: 79–89.

    CAS  Article  Google Scholar 

  7. 7

    du Cailar G, Ribstein J, Mimran A . Dietary sodium and target organ damage in essential hypertension. Am J Hypertens 2002; 15: 222–229.

    CAS  Article  Google Scholar 

  8. 8

    Matavelli LC, Zhou X, Varagic J, Susic D, Frohlich ED . Salt loading produces severe renal hemodynamic dysfunction independent of arterial pressure in spontaneously hypertensive rats. Am J Physiol Heart Circ Physiol 2007; 292: 814–819.

    Article  Google Scholar 

  9. 9

    Mattar AL, Machado FG, Fujihara CK, Malheiros DM, Zatz R . Persistent hypertension and progressive renal injury induced by salt overload after short term nitric oxide inhibition. Clinics 2007; 62: 749–756.

    Article  Google Scholar 

  10. 10

    Tian N, Gu JW, Jordan S, Rose RA, Hughson MD, Manning RD . Immune suppression prevents renal damage and dysfunction and reduces arterial pressure in salt-sensitive hypertension. Am J Physiol Heart Circ Physiol 2007; 292: 1018–1025.

    Article  Google Scholar 

  11. 11

    Rosón MI, Cavallero S, Della Penna S, Cao G, Gorzalczany S, Pandolfo M et al. Acute sodium overload produces renal tubulointerstitial inflammation in normal rats. Kidney Int 2006; 70: 1439–1446.

    Article  Google Scholar 

  12. 12

    Franco M, Martínez F, Rodríguez-Iturbe B, Johnson RJ, Santamaría J, Montoya A et al. Angiotensin II, interstitial inflammation, and the pathogenesis of salt-sensitive hypertension. Am J Physiol Renal Physiol 2006; 291: 1281–1287.

    Article  Google Scholar 

  13. 13

    Sanders PW . Effect of salt intake on progression of chronic kidney disease. Curr Opin Nephrol Hypertens 2006; 15: 54–60.

    CAS  Article  Google Scholar 

  14. 14

    Ridker PM, Hennekens CH, Buring JE, Rifai N . C-reactive protein and other markers of inflammation in the prediction of cardiovascular disease in women. N Engl J Med 2000; 342: 836–843.

    CAS  Article  Google Scholar 

  15. 15

    Shimizu K, Mitchell RN, Libby P . Inflammation and cellular immune responses in abdominal aortic aneurysms. Arterioscler Thromb Vasc Biol 2006; 26: 987–994.

    CAS  Article  Google Scholar 

  16. 16

    Sprague AH, Khalil RA . Inflammatory cytokines in vascular dysfunction and vascular disease. Biochem Pharmacol 2009; 78: 539–552.

    CAS  Article  Google Scholar 

  17. 17

    Chae CU, Lee RT, Rifai N, Ridker PM . Blood pressure and inflammation in apparently healthy men. Hypertension 2001; 38: 399–403.

    CAS  Article  Google Scholar 

  18. 18

    Lijnen PJ, Petrov VV, Fagard RH . Association between transforming growth factor-beta and hypertension. Am J Hypertens 2003; 16: 604–611.

    CAS  Article  Google Scholar 

  19. 19

    Ruiz-Ortega M, Ruperez M, Lorenzo O, Esteban V, Blanco J, Mezzano S et al. Angiotensin II regulates the synthesis of proinflammatory cytokines and chemokines in the kidney. Kidney Int 2002; 82: S12–S22.

    CAS  Article  Google Scholar 

  20. 20

    Franco V, Oparil S . Salt sensitivity, a determinant of blood pressure, cardiovascular disease and survival. J Am Coll Nutr 2006; 25: S247–S255.

    Article  Google Scholar 

  21. 21

    Obarzanek E, Proschan MA, Vollmer WM, Moore TJ, Sacks FM, Appel LJ et al. Individual blood pressure responses to changes in salt intake: results from the DASH-sodium trial. Hypertension 2003; 42: 459–467.

    CAS  Article  Google Scholar 

  22. 22

    Moore TJ, Vollmer WM, Appel LJ, Sacks FM, Svetkey LP, Vogt TM et al. Effect of dietary patterns on ambulatory blood pressure: results from the Dietary Approaches to Stop Hypertension (DASH) Trial. DASH Collaborative Research Group. Hypertension 1999; 34: 472–477.

    CAS  Article  Google Scholar 

  23. 23

    Weinberger MH . Salt sensitivity of blood pressure in humans. Hypertension 1996; 27: 481–490.

    CAS  Article  Google Scholar 

  24. 24

    Guyton AC . Dominant role of the kidneys and accessory role of whole-body autoregulation in the pathogenesis of hypertension. Am J Hypertens 1989; 2: 575–585.

    CAS  Article  Google Scholar 

  25. 25

    Guyton AC, Coleman TG . Quantitative analysis of the pathophysiology of hypertension. Circ Res 1969; 24: S1–S19.

    Article  Google Scholar 

  26. 26

    Engström G, Lind P, Hedblad B, Stavenow L, Janzon L, Lindgärde F . Long-term effects of inflammation-sensitive plasma proteins and systolic blood pressure on incidence of stroke. Stroke 2002; 33: 2744–2749.

    Article  Google Scholar 

  27. 27

    Parissis JT, Korovesis S, Giazitzoglou E, Kalivas P, Katritsis D . Plasma profiles of peripheral monocyte-related inflammatory markers in patients with arterial hypertension. Correlations with plasma endothelin-1. Int J Cardiol 2002; 83: 13–21.

    Article  Google Scholar 

  28. 28

    Miles EA, Rees D, Banerjee T, Cazzola R, Lewis S, Wood R et al. Age-related increases in circulating inflammatory markers in men are independent of BMI, blood pressure and blood lipid concentrations. Atherosclerosis 2008; 196: 298–305.

    CAS  Article  Google Scholar 

  29. 29

    Visser M, Bouter LM, McQuillan GM, Wener MH, Harris TB . Elevated C-reactive protein levels in overweight and obese adults. JAMA 1999; 282: 2131–2135.

    CAS  Article  Google Scholar 

  30. 30

    Jones-Burton C, Mishra SI, Fink JC, Brown J, Gossa W, Bakris GL et al. An in-depth review of the evidence linking dietary salt intake and progression of chronic kidney disease. Am J Nephrol 2006; 26: 268–275.

    CAS  Article  Google Scholar 

  31. 31

    Yu HC, Burrell LM, Black MJ, Wu LL, Dilley RJ, Cooper ME et al. Salt induces myocardial and renal fibrosis in normotensive and hypertensive rats. Circulation 1998; 98: 2621–2628.

    CAS  Article  Google Scholar 

  32. 32

    Tobian L, Hanlon S . High sodium chloride diets injure arteries and raise mortality without changing blood pressure. Hypertension 1990; 15: 900–903.

    CAS  Article  Google Scholar 

  33. 33

    Ying WZ, Sanders PW . Dietary salt modulates renal production of transforming growth factor-beta in rats. Am J Physiol 1998; 274: 635–641.

    Google Scholar 

  34. 34

    Ying WZ, Aaron K, Sanders PW . Mechanism of dietary salt-mediated increase in intravascular production of TGF-beta1. Am J Physiol Renal Physiol 2008; 295: 406–414.

    Article  Google Scholar 

  35. 35

    Pedrinelli R, Dell'Omo G, Di Bello V, Pellegrini G, Pucci L, Del Prato S et al. Low-grade inflammation and microalbuminuria in hypertension. Arterioscler Thromb Vasc Biol 2004; 24: 2414–2419.

    CAS  Article  Google Scholar 

  36. 36

    Tsioufis C, Dimitriadis K, Antoniadis D, Stefanadis C, Kallikazaros I . Inter-relationships of microalbuminuria with the other surrogates of the atherosclerotic cardiovascular disease in hypertensive subjects. Am J Hypertens 2004; 17: 470–476.

    CAS  Article  Google Scholar 

  37. 37

    Tsioufis C, Dimitriadis K, Chatzis D, Vasiliadou C, Tousoulis D, Papademetriou V et al. Relation of microalbuminuria to adiponectin and augmented C-reactive protein levels in men with essential hypertension. Am J Cardiol 2005; 96: 946–951.

    CAS  Article  Google Scholar 

  38. 38

    Tsioufis C, Dimitriadis K, Taxiarchou E, Vasiliadou C, Chartzoulakis G, Tousoulis D et al. Diverse associations of microalbuminuria with C-reactive protein, interleukin-18 and soluble CD 40 ligand in male essential hypertensive subjects. Am J Hypertens 2006; 19: 462–466.

    CAS  Article  Google Scholar 

  39. 39

    Stuveling EM, Bakker SJ, Hillege HL, Burgerhof JG, de Jong PE, Gans RO et alPREVEND Study Group. C-reactive protein modifies the relationship between blood pressure and microalbuminuria. Hypertension 2004; 43: 791–796.

    CAS  Article  Google Scholar 

  40. 40

    Tsioufis C, Dimitriadis K, Andrikou E, Thomopoulos C, Tsiachris D, Stefanadi E et al. ADMA, C-reactive protein, and albuminuria in untreated essential hypertension: a cross-sectional study. Am J Kidney Dis 2010; 55: 1050–1959.

    CAS  Article  Google Scholar 

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Yilmaz, R., Akoglu, H., Altun, B. et al. Dietary salt intake is related to inflammation and albuminuria in primary hypertensive patients. Eur J Clin Nutr 66, 1214–1218 (2012).

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  • albuminuria
  • hypertension
  • inflammation
  • salt intake

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