Reproducibility of salt sensitivity testing using a dietary approach in essential hypertension

Gerdts, Eva; Lund‐Johansen, Per; Omvik, Per

doi:10.1038/sj.jhh.1000814

Cited by 24 publications

(11 citation statements)

References 42 publications

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“…[17][18][19] Consistency in response was interpreted as poor, with intraclass correlation coefficients between two responses of 0.13 for ambulatory BP and 0.45 for clinic-measured mean arterial pressure. 17 Similarly, Gerdts et al 19 reported a nonsignificant correlation of 0.26 for casual and 0.02 for average 24-hour ambulatory BP when 30 participants underwent a saltsensitivity protocol twice. Other investigators reported weak statistics ranging from 0.24 to 0.38 17,18 when correlating the classifications of salt sensitivity and no salt sensitivity after conducting their protocol twice.…”

Section: Discussionmentioning

confidence: 99%

“…Investigators have interpreted data on reproducibility as either good [12][13][14][15][16] or poor. [17][18][19] Several factors may account for these contrasting interpretations, including participant differences across studies, varied duration of sodium intervention and amount of sodium levels given, sample size differences, lack of control of nutrients other than sodium, or lack of consensus as to what constitutes "good" reproducibility. Alternatively, one can view the mixed results as an indication that individual BP response to salt varies, in part randomly.…”

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confidence: 99%

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Individual Blood Pressure Responses to Changes in Salt Intake

et al. 2003

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Abstract-Although group characteristics are known to influence average blood pressure response to changes in salt intake, predictability of individual responses is less clear. We examined variability and consistency of individual systolic blood pressure responses to changes in salt intake in 188 participants who ate the same diet at higher, medium, and lower (140, 104, 62 mmol/d) sodium levels for 30 days each, in random order, after 2 weeks of run-in at the higher sodium level.Regarding variability in systolic blood pressure changes over time, changes from run-in to higher sodium (no sodium level change) ranged from Ϫ24 to ϩ25 mm Hg; 8.0% of participants decreased Ն10 mm Hg. Regarding variability in systolic blood pressure response to change in sodium intake, with higher versus lower sodium levels (78-mmol sodium difference), the range of systolic blood pressure change was Ϫ32 to ϩ17 mm Hg; 33.5% decreased Ն10 mm Hg.Regarding consistency of response, systolic blood pressure change with run-in versus lower sodium was modestly correlated with systolic blood pressure change with higher versus medium sodium; systolic blood pressure change with higher versus lower sodium was similarly correlated with run-in versus medium sodium (combined Spearman rϭ0.27, Pϭ0.002). These results show low-order consistency of response and confirm that identifying individuals as sodium responders is difficult. They support current recommendations for lower salt intake directed at the general public rather than "susceptible" individuals as one of several strategies to prevent and control adverse blood pressures widely prevalent in the adult population. Key Words: blood pressure Ⅲ systole Ⅲ sodium, dietary Ⅲ blood pressure determination E vidence for a relation between salt and blood pressure (BP) has accumulated for over 50 years. 1 Animal studies, 2 cross-country ecological studies, 1,3 epidemiologic studies of individuals, 4,5 randomized trials, 6,7 and meta-analyses of trials 8 show that salt intake is directly related to BP and that lowering salt intake lowers BP.In addition to examining group average BP responses to salt intake, researchers have reported that BPs of some individuals fall with reduction in salt intake, but BPs of others do not (ie, interindividual differences in BP response), leading to the concept of salt sensitivity in individuals. Conclusions regarding salt sensitivity have been generally based on observations of BP responses in individuals who have undergone an experimental protocol only once. These protocols varied sodium intake and/or excretion over a period of time, often for only a few days or 1 to 2 weeks, and sometimes used extreme variations in salt intake. 9 -11 Although one-time individual BP responses to sodium reduction have a continuous distribution, investigators have interpreted these data dichotomously, responders and nonresponders, based on arbitrarily defined cut-points. These interpretations led to suggestions that strategies for reduced sodium intake be directed at "susceptible" individuals r...

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Section: Discussionmentioning

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Individual Blood Pressure Responses to Changes in Salt Intake

et al. 2003

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“…10,11,18,33 In contrast to previous studies that used a single baseline measurement of urinary salt excretion or the average of the measurements on follow-up, 34 in our time-dependent Cox model we used, for the first time in this clinical setting, a cumulative average of sodium excretion. This is a gold-standard approach to model the relationship between longitudinally measured covariates and a given event 35 that has been extensively applied in Figure 4.…”

Section: Monitoring Salt Intakementioning

confidence: 99%

Sodium Intake, ACE Inhibition, and Progression to ESRD

Vegter

Perna

Postma

et al. 2012

Journal of the American Society of Nephrology

278

179

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High sodium intake limits the antihypertensive and antiproteinuric effects of angiotensin-converting enzyme (ACE) inhibitors in patients with CKD; however, whether dietary sodium also associates with progression to ESRD is unknown. We conducted a post hoc analysis of the first and second Ramipril Efficacy in Nephropathy trials to evaluate the association of sodium intake with proteinuria and progression to ESRD among 500 CKD patients without diabetes who were treated with ramipril (5 mg/d) and monitored with serial 24-hour urinary sodium and creatinine measurements. Urinary sodium/creatinine excretion defined low (,100 mEq/g), medium (100 to ,200 mEq/g), and high ($200 mEq/g) sodium intake. During a follow-up of .4.25 years, 92 individuals (18.4%) developed ESRD. Among those with low, medium, and high sodium intakes, the incidence of ESRD was 6.1 (95% confidence interval [95% CI], 3.8-9.7), 7.9 (95% CI, 6.1-10.2), and 18.2 (95% CI, 11.3-29.3) per 100 patient-years, respectively (P,0.001). Patients with high dietary sodium exhibited a blunted antiproteinuric effect of ACE inhibition despite similar BP among groups. Each 100-mEq/g increase in urinary sodium/creatinine excretion associated with a 1.61-fold (95% CI, 1.15-2.24) higher risk for ESRD; adjusting for baseline proteinuria attenuated this association to 1.38-fold (95% CI, 0.95-2.00). This association was independent from BP but was lost after adjusting for changes in proteinuria. In summary, among patients with CKD but without diabetes, high dietary salt (.14 g daily) seems to blunt the antiproteinuric effect of ACE inhibitor therapy and increase the risk for ESRD, independent of BP control.

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“…Inasmuch as this problem has been addressed, results are variable and there is certainly no stone-hard evidence that the phenomenon is reproducible. 5,6 However, the studies that have been done have included only a small number of individuals and spanned a relatively short period of time. Therefore, it is very fortunate and timely that this issue of Hypertension features a study by Gu et al 7 on the long-term reproducibility of salt-sensitivity testing.…”

Section: See Related Article P 499-505mentioning

confidence: 99%

Salt and Sensitivity

Leeuw

2013

Hypertension

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Reproducibility of salt sensitivity testing using a dietary approach in essential hypertension

Cited by 24 publications

References 42 publications

Individual Blood Pressure Responses to Changes in Salt Intake

Individual Blood Pressure Responses to Changes in Salt Intake

Sodium Intake, ACE Inhibition, and Progression to ESRD

Salt and Sensitivity

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