ADMA, C-Reactive Protein, and Albuminuria in Untreated Essential Hypertension: A Cross-sectional Study

Tsioufis, Costas; Dimitriadis, Kyriakos; Andrikou, Eirini; Thomopoulos, Costas; Tsiachris, Dimitris; Stefanadi, Elli; Mihas, Costas; Miliou, Antigoni; Papademetriou, Vasilios; Stefanadis, Christodoulos

doi:10.1053/j.ajkd.2009.11.024

Cited by 57 publications

(49 citation statements)

References 38 publications

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“…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.…”

Section: Discussionmentioning

confidence: 47%

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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Section: Discussionmentioning

confidence: 47%

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

et al. 2012

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“…Indeed, in acute sepsis, ADMA is downregulated (34), whereas high ADMA levels are consistently associated with biomarkers of inflammation in a variety of chronic conditions including untreated essential hypertension (35), glucose intolerance (36), familial Mediterranean fever (33), and inflammatory bowel diseases (37). In vitro, ADMA induces TNF-␣ production via reactive oxygen species/NF-B-dependent pathway (38).…”

Section: Interaction Between Adma and Inflammationmentioning

confidence: 99%

Inflammation and Asymmetric Dimethylarginine for Predicting Death and Cardiovascular Events in ESRD Patients

Tripepi¹,

Mattace-Raso

Sijbrands

et al. 2011

Clinical Journal of the American Society of Nephrology

106

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SummaryBackground Endothelial dysfunction as assessed by asymmetric dimethylarginine (ADMA) and inflammation has been consistently linked to atherosclerosis, death, and cardiovascular (CV) events in ESRD patients. Inflammation amplifies the effect of ADMA on the severity of atherosclerosis in ESRD patients, but it is still unknown whether inflammation and ADMA interact in the high risk of death and CV events in this population. Design, setting, participants, & measurementsIn a cohort of 225 hemodialysis patients, we investigated the interaction between inflammatory biomarkers (C-reactive protein and IL-6) and ADMA as predictors of death and CV events over an extended follow-up (13 years).Results During follow-up, 160 patients died, and 123 had CV events. With crude and multiple Cox regression analyses, an interaction was found between inflammation biomarkers and ADMA for explaining death and CV events in ESRD patients. The adjusted hazard ratios (HRs) for death (HR, 2.18; 95% confidence interval [CI], 1.34 to 3.54) and CV outcomes (HR, 2.59; 95% CI, 1.47 to 4.55) of patients with C-reactive protein and ADMA above the median were higher than expected in the absence of interaction under the additive model (1.15 and 1.97, respectively) and significantly higher than in patients with only one biomarker above the median. Data analyses carried out by stratifying patients according to IL-6 provided similar results. ConclusionsThese data support the hypothesis that inflammation amplifies the risk of death and CV events associated with high ADMA levels in ESRD. These analyses further emphasize the need for intervention studies to attenuate inflammation and high ADMA levels in this population.

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“…10 Inflammation seems to have a pivotal role in the pathogenesis of hypertension and hypertensive target organ damage. In these lines, we have recently shown that high-sensitivity CRP (hs-CRP) is associated with microalbuminuria, 11 whereas increased hs-CRP and decreased adiponectin levels go together with a state of increased aortic stiffness in hypertensives. 12 In addition, SUA seems to have a bidirectional relationship with inflammation, and it is unclear whether uric acid has anti-oxidant or prooxidant effects.…”

Section: Introductionmentioning

confidence: 99%

The diverse associations of uric acid with low-grade inflammation, adiponectin and arterial stiffness in never-treated hypertensives

et al. 2010

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The data regarding the role of serum uric acid (SUA) along with subclinical inflammation in the context of hypertensive vascular damage are rather scarce and controversial. Towards this end, we assess the links between SUA, high-sensitivity CRP (hs-CRP), adiponectin and carotid to femoral pulse wave velocity (c-f PWV) in 292 subjects with never-treated stage I-II essential hypertension. On the basis of the median SUA levels (0.31 mmol l À1 ), the study population was divided into subjects with low (n ¼ 149) and high (n ¼ 143) SUA values. By multiple regression analysis, it was revealed that SUA was independently associated with log hs-CRP (R 2 ¼ 0.098; P ¼ 0.02), log adiponectin (R 2 ¼ 0.102; P ¼ 0.03), waist circumference (R 2 ¼ 0.049; P ¼ 0.04), 24-h systolic blood pressure (SBP) (R 2 ¼ 0.179; P ¼ 0.001) and estimated glomerular filtration rate (R 2 ¼ 0.156; b (s.e.) ¼ À0.169 (0.023); P ¼ 0.02). In addition, c-f PWV was independently associated with age (R 2 ¼ 0.116; Po0.0001), waist circumference (R 2 ¼ 0.088; Po0.0001), 24-h SBP (R 2 ¼ 0.167; P ¼ 0.001), log adiponectin (R 2 ¼ 0.07; P ¼ 0.006) and log hs-CRP (R 2 ¼ 0.06; P ¼ 0.034). In conclusion, SUA levels are independently associated with hs-CRP and adiponectin levels but not with c-f PWV in essential hypertensive patients. Increased SUA levels are accompanied by a state of pronounced inflammatory activation and hypoadiponectinemia that significantly impairs the arterial stiffness accelerating the vascular ageing process in this setting.

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ADMA, C-Reactive Protein, and Albuminuria in Untreated Essential Hypertension: A Cross-sectional Study

Cited by 57 publications

References 38 publications

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

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

Inflammation and Asymmetric Dimethylarginine for Predicting Death and Cardiovascular Events in ESRD Patients

The diverse associations of uric acid with low-grade inflammation, adiponectin and arterial stiffness in never-treated hypertensives

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