Immune suppression prevents renal damage and dysfunction and reduces arterial pressure in salt-sensitive hypertension

Tian, Niu; Gu, Jingang; Jordan, Sharkeshia; Rose, Rebecca; Hughson, Michael D.; Manning, R. Davis

doi:10.1152/ajpheart.00487.2006

Cited by 87 publications

(79 citation statements)

References 32 publications

(46 reference statements)

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“…Finally, a recent cross-sectional study found that highdietary salt intake was associated with both increased albuminuria and C-reactive protein in treated patients with hypertension (43), suggesting that inflammatory mechanisms might also be involved in the nephrotoxic effect of excess salt intake (44,45).…”

Section: Possible Mechanisms Of the Effect Of Sodium Intake Reductionmentioning

confidence: 99%

Meta-Analysis of the Effect of Dietary Sodium Restriction with or without Concomitant Renin-Angiotensin-Aldosterone System–Inhibiting Treatment on Albuminuria

D’Elia¹,

Rossi²,

Cola³

et al. 2015

Clinical Journal of the American Society of Nephrology

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Background and objectives Urinary albumin excretion and/or albumin to creatinine ratio are associated with CKD and higher risk of cardiovascular events. Several studies investigated the effect of reduced dietary sodium intake on urinary albumin excretion and/or albumin to creatinine ratio in adult patient populations, but the majority was inconclusive because of insufficient statistical power. A meta-analysis of the randomized, controlled trials available could overcome this problem and lead to more definitive conclusions.Design, setting, participants, & measurements A systematic search of the online databases available (from 1996 to October of 2014) was conducted of randomized, controlled trials that expressed urinary albumin excretion or albumin to creatinine ratio as the difference between the effects of two different sodium intake regimens. For each study, the mean difference and 95% confidence intervals were pooled using a random effect model. Heterogeneity, publication bias, subgroup, and meta-regression analyses were performed.Results Eleven studies met the predefined inclusion criteria and provided 23 cohorts with 516 participants and 1-6 weeks of follow-up time. In the pooled analysis, an average reduction in sodium intake of 92 mmol/d was associated with a 32.1% (95% confidence interval, 244.3 to 218.8) reduction in urinary albumin excretion. The effect of sodium restriction was higher in the cohorts including patients on concomitant renin-angiotensin-aldosterone system-blocking therapy, in the studies with intervention lasting at least 2 weeks, and among participants with evidence of kidney damage. A greater reduction of urinary albumin excretion was associated with a higher decrease in BP during the intervention. The analysis of changes in albumin to creatinine ratio provided similar results.Conclusions This meta-analysis indicates that sodium intake reduction markedly reduces albumin excretion, more so during concomitant renin-angiotensin-aldosterone system-blocking therapy and among patients with kidney damage.

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Section: Possible Mechanisms Of the Effect Of Sodium Intake Reductionmentioning

confidence: 99%

Meta-Analysis of the Effect of Dietary Sodium Restriction with or without Concomitant Renin-Angiotensin-Aldosterone System–Inhibiting Treatment on Albuminuria

D’Elia¹,

Rossi²,

Cola³

et al. 2015

Clinical Journal of the American Society of Nephrology

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“…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.…”

Section: Introductionmentioning

confidence: 99%

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

et al. 2012

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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), mediumsalt-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. 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][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. 9-13 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...

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“…High circulating IL6, TNF-α, IL8 and MCP1 were detected in a cross-sectional study of 275 stable hypertensive patients with or without HFpEF [48]. In salt sensitive hypertension, high salt intake leads to systemic oxidative stress [101] possibly because of renal production of proinflammatory cytokines [102]. The RAAS is a major activator of NADPH oxidase and reactive oxygen species (ROS) production and increasing evidence reveals that the RAAS is importantly involved in linking obesity, metabolic syndrome, insulin resistance (IR), chronic kidney disease and hypertension [103].…”

Section: Hypertensionmentioning

confidence: 99%

Impact of Comorbidities on Myocardial Remodeling and Dysfunction In Heart Failure with Preserved Ejection Fraction

Heerebeek

Paulus²

2014

SOJPPS

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Immune suppression prevents renal damage and dysfunction and reduces arterial pressure in salt-sensitive hypertension

Cited by 87 publications

References 32 publications

Meta-Analysis of the Effect of Dietary Sodium Restriction with or without Concomitant Renin-Angiotensin-Aldosterone System–Inhibiting Treatment on Albuminuria

Meta-Analysis of the Effect of Dietary Sodium Restriction with or without Concomitant Renin-Angiotensin-Aldosterone System–Inhibiting Treatment on Albuminuria

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

Impact of Comorbidities on Myocardial Remodeling and Dysfunction In Heart Failure with Preserved Ejection Fraction

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