Assessment Of Sodium Intake Research Articles

Development of a Formula for Estimation of Sodium Intake from Spot Urine in People with Chronic Kidney Disease

Background/Aims: High sodium intake is associated with adverse cardiovascular and renal outcomes in people with chronic kidney disease (CKD), and simple methods to facilitate assessment of sodium intake are required. The objective of this study was to develop a new formula to estimate 24-hour urinary sodium (24hUNa) excretion from urinary Na concentration measured on an early morning urine specimen (EM UNa). Methods: Seventy participants from a prospective cohort of patients with CKD stage 3 in primary care, the Renal Risk in Derby (RRID) study, agreed to collect an additional EM UNa on the day after completing a 24-hour urine collection. A formula to estimate 24hUNa from EM UNa and body weight was developed using the coefficients from a multivariable linear regression equation. The accuracy of the formula was tested by calculating the P30 (proportion of estimates within 30% of measured sodium exection), and the ability of the estimated 24hUNa to discriminate between measured sodium intake above or below 100 mmol/day was assessed by receiver operating characteristic (ROC) curve. A Bland-Altman plot was used to estimate the bias and limits of agreement between estimated and measured 24hUNa. Seventy-four additional paired 24hUNa and EM UNa from 50 CKD stage 3 patients in the RRID study were used to validate the formula. Results: The mean difference between measured and estimated 24hUNa was 2.08 mmol/day. Measured and estimated 24hUNa were significantly correlated (r = 0.55; p < 0.001) but accuracy of estimated 24hUNa was low (P30 = 60%). Analysis of the ROC curve with a cut-off point >100 mmol/day yielded an area under the curve of 0.668, sensitivity of 0.85 and specificity of 0.52. Conclusions: We have developed a simple formula to identify people with a high sodium intake from EM UNa, suitable for use in large-cohort or population studies.

Sodium and cardiovascular disease: what the data show.

Considerable attention has been devoted to interpretation of cohort analyses used to study the relationship between sodium (Na) intake and cardiovascular disease (CVD). Reports have included analyses from individual studies, systematic reviews of the literature, and meta-analyses. Recently, Graudal et al. published a meta-analysis and concluded, “Both low sodium intakes and high sodium intakes are associated with increased mortality, consistent with a U-shaped association between sodium intake and health outcomes.” 1 Before accepting this statement, one should consider the quality of the underlying studies, the appropriateness of pooling the data, study-specific methodologi cal issues, results of cohort studies not included in Graudal et al.’s meta-analysis, evidence from randomized controlled trials (RCTs), and the consistency of Graudal et al.’s conclusion with those of other investigators. Quality of the underlying studies Every cohort analysis that has explored the relationship between Na and CVD (Na–CVD) was based on secondary examination of data from studies not originally designed to investigate the association. All were subject to methodological challenges, 2 including the potential for systematic bias in measurement of Na, reverse causality, and imprecision of urinary Na estimates. A recent systematic review of 31 independent Na–CVD analyses, based on experience in 26 cohorts, identified a direct association in 13 analyses (42%), a J-shaped curve in 2 (6%), a null relationship in 8 (26%), and an inverse relationship in the remaining 8 (26%). 3 On average, there were 3–4 methodological issues per study. Issues with greater and lesser potential to alter the direction of the association were noted in 96% and 69% of the studies, respectively, whereas issues with the potential to yield false-negative results were noted in 88%. Na intake was estimated by means of 24-hour recall or food frequency instruments in 15 (58%) of the studies, with only a single observation used in 13 (87%) of the 15 studies. Use of goldstandard 24-hour urine estimates was restricted to 9 (35%) of the studies, and all but 2 4,5 were based on use of a single 24-hour urine collection. A recent Na balance study identified an astounding degree of day-to-day variation in urinary Na excretion, 6 underscoring the importance of estimation based on an average derived from multiple 24-hour urine collections. These issues have led several review panels to express seri ous concerns about the quality of the cohort data that have been used to assess the relationship between Na intake and CVD. The authors of the previously mentioned systematic review 3 judged the quality of the data as substandard and felt methodological issues might account for the inconsistent findings from these studies. Others have reached a similar conclusion. A 2013 Institute of Medicine (IOM) Committee report found the studies “were highly variable in methodological quality, particularly in assessing sodium intake.” 7 A 2012 World Health Organization (WHO) report noted a significant direct relationship between Na and stroke but using GRADE methodology identified the quality of the evi dence as “very low.” 8

Circulation : Clinical Summaries

<i>Circulation</i> : Clinical Summaries

Salt intakes and salt reduction initiatives in Southeast Asia: a review.

Increased dietary sodium intake is a modifiable risk factor for cardiovascular disease. The monitoring of population sodium intake is a key part of any salt reduction intervention. However, the extent and methods used for as-sessment of sodium intake in Southeast Asia is currently unclear. This paper provides a narrative synthesis of the best available evidence regarding levels of sodium intake in six Southeast Asian countries: Indonesia, Malaysia, Philippines, Singapore, Thailand, Vietnam, and describes salt reduction measures being undertaken in these countries. Electronic databases were screened to identify relevant articles for inclusion up to 29 February 2012. Reference lists of included studies and conference proceedings were also examined. Local experts and researchers in nutrition and public health were consulted. Quality of studies was assessed using a modified version of the Downs and Black Checklist. Twenty-five studies fulfilled the inclusion criteria and were included in this review. Full texts of 19 studies including government reports were retrieved, with most studies being of good quality. In-sufficient evidence exists regarding salt intakes in Southeast Asia. Dietary data suggest that sodium intake in most SEA countries exceeded the WHO recommendation of 2 g/day. Studies are needed that estimate sodium intake using the gold standard 24-hour urinary sodium excretion. The greatest proportion of dietary sodium came from added salt and sauces. Data on children were limited. The six countries had salt reduction initiatives that differed in specificity and extent, with greater emphasis on consumer education.

Assessing U.S. sodium intake through dietary data and urine biomarkers.

Sodium intake is related to blood pressure, an established risk factor for heart disease and stroke. Reducing intake may save billions in United States health care dollars annually. Efforts targeting sodium reductions make accurate monitoring vital, yet limited information exists on the accuracy of the current data to assess sodium intake in the United States population. In this symposium, new findings were presented on the accuracy of estimating population 24-h urinary excretion of sodium from spot urine specimens or sodium intake from 24-h dietary recalls. Differences in accuracy by sex, BMI, and race were apparent as well as by timing of spot urine collections. Although some published equations appear promising for estimating group means, others are biased. Individual estimates of sodium intake were highly variable and adjustment for within-individual variation in intake is required for estimating population prevalence or percentiles. Estimates indicated United States sodium intake remains high.

Trend in sources of sodium in the US diet over the last decade: Analysis of What We Eat In America (WWEIA)/National Health and Nutrition Examination Survey (NHANES) 2001–2010

WWEIA data were used to assess sodium intake and sources in the diets of those 2+ years of age (N=42,151) over the last decade. Regression analyses were conducted to determine a p‐for trend across the five NHANES data releases, 2001–2010. Average, covariate adjusted, sodium intake over the decade was 3406 ± 9 mg/d. Major contributors of sodium (mean ± SE, mg/d) in the diet across the decade were Grains (1317 ± 10); Meat, Poultry, Fish (MPF) and Mixtures (985 ± 10); Vegetables (393 ± 6); and Milk and Milk Products (293 ± 3). Sodium intake has increased across the decade by 63 mg/d per 2 yr release (p‐for trend &lt;0.0001). The largest increase in sodium was from MPF and Mixtures (45 mg/d per release, p&lt;0.0001) with Poultry increasing 20.3 mg/d (p&lt;0.0001) and MPF with Nonmeat Items increasing 14.1 mg/d (p&lt;0.05) per release, respectively. There were smaller increases in Vegetables (10 mg/d per release, p&lt;0.05) and Sugars, Sweets, and Beverages (11 mg/d per release, p&lt;0.001). There was also a small, but significant, decrease in sodium from Fats, Oils, and Salad Dressings (7 mg/d per release, p&lt;0.0001).While sodium from Grains was consistent across the releases, White Bread, Rolls and Salty Snacks From Grain Products decreased 9.2 (p&lt;0.0001) and 4.2 (p&lt;0.05) mg/d per release while Mixtures Mainly Grain, Pasta, or Bread increased 14.1 mg/d per release, respectively. Sodium intakes have continued to increase over the last 10 years and solutions to help decrease dietary intakes are greatly needed. Funded by Tate &amp; Lyle Health &amp; Nutrition Sciences.

Assessment of salt intake: how accurate is it?

The aims of this review paper are to provide an overview of the association of sodium intake with cardiovascular health, to identify sodium in our global food supply and to describe problems associated with assessment of dietary sodium intake. Excess sodium intake may contribute to the development of hypertension in some individuals, consequently increasing CVD risk. The average intake of sodium in populations around the world far exceeds the actual body's needs. Processed and restaurant foods contribute the most dietary sodium for Americans and other populations worldwide. There is a worldwide focus on reducing sodium content of food products in an effort to reduce health related issues associated with excessive salt and sodium intake in individuals. In several countries, regulations have been introduced to lower the sodium content of foods. Manufacturers are complying with these regulations by formulating new products to meet these standards. However, the variability in food sodium content poses challenges to researchers to accurately assess dietary sodium intakes of individuals. There are differences in sodium content of foods in databases compared with nutritional information provided by manufacturers for the same food products. Variations also exist in restaurant foods, where values differ from those available on restaurant websites. Sodium may be either underestimated or overestimated; it is not always on target. Awareness of the variability among food products is crucial but capturing sodium content of every food in the market is not feasible. Whenever possible, updating databases is critical. In conclusion, it is not feasible to capture the sodium content of every food in the marketplace but being aware of these differences is essential to assessing actual sodium consumption. Since biological determinations are burdensome and impractical, it is imperative for researchers and other health professionals to participate in the development and implementation of tools to accurately assess sodium intake in individuals.

USDA Monitors Levels of Added Sodium in Commercial Packaged and Restaurant Foods

This manuscript describes progress by the Nutrient Data Laboratory (NDL) in monitoring sodium in processed and prepared foods frequently consumed by the U.S. population. Recent concerns by the U.S. public health community about the intake of sodium by Americans have led ARS, USDA to develop a plan to monitor the levels of sodium in highly consumed commercial packaged and restaurant foods. NDL scientists worked with USDA's Food Surveys Research Group (FSRG) to identify 125 Sentinel Foods, to serve as indicators for assessment of change in the sodium content in the food supply. For each food (e.g., cheese pizza) NDL used market share data to identify the predominant brands and types of foods (e.g., frozen cheese pizza, restaurant pizza) to be monitored for changes in the sodium level over time. Periodically, nutrient values for frequently consumed foods will be updated by chemical analysis or label checks. Estimates will be compared to existing values in the National Nutrient Database for Standard Reference (SR). Since 2010, about 140 foods have been sampled and analyzed by NDL contractors. NDL will continue to generate new sodium data which will be disseminated in the successive releases of the SR. Accurate and current data for sodium in processed foods will support the assessment of changes in sodium in foods as well as the assessment of sodium intake by the U.S. population in the years ahead.

Resistant hypertension and the neglected antihypertensive: sodium restriction

Resistant hypertension is defined as blood pressure (BP) that remains above goal (such as 140/90 mmHg or more) in spite of the concurrent use of three antihypertensive agents of different classes. Ideally, one of the three agents should be a diuretic and all agents should be prescribed at optimal dose amounts. Prevalent among 15% of the treated hypertensives, the risk factors for resistant hypertension include older age, chronic kidney disease (CKD), obesity and diabetes mellitus. Causes of resistant hypertension can be classified into four groups: poor adherence, biological-behavioral factors, CKD and secondary causes, and drugs or exogenous substances. However, before labeling the diagnosis of resistant hypertension, it is important to exclude pseudo-resistant hypertension using home BP monitoring in most patients and ambulatory BP monitoring in a few. Before thinking about the next antihypertensive drug, it is important to restrict dietary sodium. Educating the patient on how to interpret the food label and providing feedback by assessing sodium intake with 24 h urine collection are effective sodium restriction strategies. Sodium restriction can lower BP and among patients with proteinuria can even enhance the anti-proteinuric effects of drugs that block the renin-angiotensin system. Sodium restriction is therefore a valuable but a neglected antihypertensive.

Evaluation of 2 methods for sodium intake assessment in cardiac patients with and without heart failure: the confounding effect of loop diuretics

Twenty-four-hour urine collections are considered the optimal method for sodium intake assessment. Whether a diagnosis of heart failure (HF) or the use of loop diuretic (LD) therapy for HF compromises the validity of 24-h urine collections as a surrogate marker for sodium intake is unknown. The objective was to determine the strength of association between 24-h urine collections and food records for sodium intake assessment in non-HF cardiac patients and in HF patients stratified by LD usage. Food records and 24-h urine collections were simultaneously completed for 2 consecutive days. Correlation coefficients and the Bland-Altman method of agreement described the relation between the techniques. Non-HF cardiac patients (n = 96; mean ± SD age: 65 ± 11 y), HF patients who were not taking an LD (n = 47; 62 ± 11 y), and HF patients who were taking an LD (n = 62; age: 60 ± 12 y) were included. Correlation coefficients for sodium intake between food records and urine collections were r = 0.624 (P < 0.001) for non-HF cardiac patients and r = 0.678 (P < 0.001) for HF patients who were not taking an LD. However, no significant association (r = 0.132, P = 0.312) was observed for HF patients who were taking LDs. The 95% limits of agreement between the non-HF cardiac patients and the HF patients who were not taking LDs were similar but were ≈50% wider for HF patients who were taking LDs. For the assessment of sodium intake, food records agree well with 24-h urine collections in non-HF patients with cardiovascular disease and in HF patients who are not receiving LD but not for HF patients who are taking LDs. Therefore, food records may provide a better estimate of sodium intake in HF patients who are receiving LD therapy.

Development and use of FFQ among adults in diverse settings across the globe

In nutritional epidemiology, development of valid dietary assessment instruments specific to populations in diverse settings is of paramount importance. Such instruments are essential when trying to characterise dietary patterns and intake, investigate diet-disease associations, inform and evaluate nutrition interventions, assess nutrient-gene interactions, conduct cross-country comparison studies and monitor nutrition transitions. The FFQ is a relatively inexpensive tool for measuring long-term dietary intake for large populations and for allowing researchers to track dietary changes over time. However, FFQ must be population specific to capture the local diet and available foods. Collecting 24-h dietary recalls and utilising community feedback to build the FFQ ensures that a culturally appropriate instrument is developed. This article presents several examples describing FFQ development and utilisation in different settings globally. In the Canadian Arctic, FFQ were developed and utilised to inform and evaluate a community-based intervention programme, characterise the diet and track dietary changes occurring among Inuit and Inuvialuit, populations experiencing rising rates of chronic disease and likely to be extremely vulnerable to the potential effects of climate change. Another example is an FFQ developed to assess sodium intake and evaluate a sodium reduction trial in a high-risk population in Barbados. An example is provided from Brazil, where an FFQ was developed to assess associations between diet, heterocyclic aromatic amines and colorectal adenoma among Japanese Brazilians and to conduct cross-country comparisons. These and other case studies highlight the diversity in dietary intake between populations and the need for FFQ to be developed to capture this diversity.

Estimation of 24‐Hour Sodium Excretion from Spot Urine Samples

Despite the effects of sodium intake on blood pressure and on response to antihypertensive medication, sodium intake is rarely monitored in clinical practice. The current method, the 24-hour urine collection for sodium excretion, is cumbersome, often incorrectly performed, and not commonly ordered. Further, its results have limited meaning because of the substantial day-to-day variation in sodium intake. A spot urine test to enable convenient, inexpensive, and serial monitoring of sodium excretion would be desirable. In this study, the accuracy of predicting 24-hour sodium excretion from a spot urine sample was assessed. The urine sodium/creatinine ratio was determined from the following urine samples: an "AM sample," submitted at the beginning of the 24-hour urine collection; a "PM sample" collected in the later afternoon/early evening before dinner, at roughly the midpoint of the collection; and a "random sample," collected after its completion. The ratio was then corrected for 24-hour creatinine excretion. The strongest correlation between predicted and actual 24-hour sodium excretion was observed with the PM sample collected near the midpoint (r=0.86, P<.001). This sample also identified persons with sodium excretion <100 mEq/d with a sensitivity of 100% and specificity of 82%. The sodium/creatinine ratio from a spot urine sample collected in the late afternoon/early evening at roughly the midpoint of the 24-hour collection, and adjusted for 24-hour creatinine excretion, strongly correlated with 24-hour sodium excretion. Additional studies are merited to further evaluate the role of the spot urine sample in assessing sodium intake.

Sodium Intake and Mortality: The Debate Continues

Dietary patterns have long been recognized as a key factor in the association of disease patterns and health outcomes. Pellagra, as an example, was prevalent among the poor in the American South in the early 1900s and was basically eradicated with nutritious diets and vitamin-enriched flour.1,2 Other conditions such as scurvy are well recognized as associated with diet and malnutrition, and recognized currently in developing countries.3 Similarly, the high intake of dietary cholesterol and fats was found decades ago to be associated with increased risks of cardiovascular disease. 4,5 These findings have led to public health interventions and policies designed to improve dietary patterns in an effort to promote health and prevent disease. The dietary intake of salt and sodium represents another major lifestyle and behavior associated with disease prevalence. The associations of sodium intake and adverse cardiovascular outcomes have long been recognized, with reduction in salt consumption considered a major public health intervention. Reduction in sodium intake is a recommended lifestyle modification of the Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure: (JNC 7 report)6 for all stages of elevated blood pressure. In many clinical investigations, sodium reduction was associated with blood pressure lowering among hypertensives, both alone and as a complement to medical treatment.7 The information regarding the risks of high sodium intake and the potential benefit of a lower sodium diet has been conveyed effectively to the public. In a study of older Americans regarding attitudes on lifestyle and blood pressure level, 90% of the respondents reported that a reduction in salt intake was effective for treating and controlling high blood pressure, with 14% indicating sodium restriction as the most effective lifestyle factor.8 However, with a society skeptical of strategies that fail to yield proclaimed benefits, it is prudent for clinical investigators and epidemiologists to quantify accurate risks and benefits. In this issue of the Journal of General Internal Medicine, Cohen and colleagues continue the debate regarding the risks and benefits of salt intake.9 In particular, the authors assess cardiovascular disease and all-cause mortality in the Third National Health and Nutrition Examination Survey (NHANES III) determining modest and non-significant association of sodium intake and higher mortality risks. Further, they concluded from the analyses that higher sodium intake was unlikely to be an independent predictor of high cardiovascular or all-cause mortality.9 While the analyses are reasonable and take advantage of a valuable epidemiologic data base, several issues should be considered when evaluating the results. First, these results are based on a secondary data analysis. While such results are valuable in developing hypotheses, conclusions are better based on randomized clinical trials.10 The assessment of sodium intake is another limitation of the study, as indicated by the authors. The use of a single measure of sodium intake as an indication of salt consumption may indeed not be representative of the true diet. Likewise, this concern is multiplied as there are no sodium excretion measures to validate the intake values. A third issue regards the potential sampling issues of the NHANES III, which was not designed specifically for the measurement of sodium intake in the population. While this is an excellent study cohort, inclusion of individuals with varying geographic and cultural use of salt may not be adequately sampled. These parameters were not included in the statistical models. When Alderman and colleagues presented earlier work in 1998 with similar findings using the first National Health and Nutrition Examination Survey,11 conflicting views were expressed. The spirited exchange of letters identified many of the limitations and cautions described with the current paper, with the references to numerous epidemiological studies reporting the benefits of salt reduction. Thus, the debate continues. However, as the clinical guidelines for disease management and policies regarding sodium are updated, it is imperative these documents be based on actuate information. While the debate is “healthy” for the progress of science, it can be confusing when affecting prevention and disease management strategies.

High sodium intake modulates left ventricular mass in patients with G expression of +1675 G/A angiotensin II receptor type 2 gene

In patients with hypertension left ventricular hypertrophy (LVH) is associated with genetic variations of the angiotensin type 2 receptor (AT2R). Hypertension and LVH are often aggravated by salt intake. Our objective was to assess the relationship between AT2R gene variation and salt intake and their impact on left ventricular mass (LVM). In 205 subjects with normal or mildly elevated blood pressure, we assessed sodium intake and left ventricular structure and function by echocardiography. Intronic +1,675 G/A polymorphism of the AT2R gene was investigated. A-allele carriers had a greater LVM (P = 0.049) than G-allele carriers. Independent of diet, septal wall thickness was higher in A-allele carriers (P = 0.001). Fractional fibre shortening was greater in A-allele carriers (P = 0.034), and the velocity of circumferential fibre shortening tended to be greater in A-allele carriers (P = 0.057). When the two groups were stratified according to their salt intake, only G-allele carriers displayed a modulating effect of salt intake on LVM. Covariance analysis revealed that there was a trend towards a modulating effect of salt intake on LVM, even after taking blood pressure into account (P = 0.054). Our data clearly support the notion that LVM is influenced by AT2R polymorphisms. Furthermore, G-allele carriers in particular appear to be susceptible to a modifying effect of increased salt intake on LVM.

Salt usage behaviors are related to urinary sodium excretion in normotensive Korean adults.

High sodium intake is considered to be the major risk factor for hypertension but studies about sodium intake on prevention and management of hypertension is limited due to the difficulties in assessment of sodium intake. Dietary sodium comes not only from naturally occurring sodium in foods but also from the added sodium during processing, cooking and at the table. Present study was conducted to identify salt usage behavior questions related to urinary sodium excretion among normotensive adult Koreans. The test version of the salt usage questionnaire included six items of salt usage behaviors and nine items of high salt containing foods. A survey was conducted in 189 adults over 18 years of age in three age groups in both genders. Each participant answered the questionnaire and collected one 24-hour urine and urine samples were analyzed for sodium contents. Correlation analyses between scores of the questions and sodium excretion in 24-hour urine were performed to identify question items related to sodium excretion. Among fifteen questions, scores of three questions on salt usage behaviors were significantly correlated to urinary sodium excretion (r=0.17~0.19; p <0.05) and the sum of scores of the three questions showed higher correlation coefficients. (r=0.26, p <0.001) The salt usage behavior questions developed in this study would be useful in predicting sodium intake and in studying the relationship between sodium intake and health among Korean adults.

Sodium in the Finnish diet: II Trends in dietary sodium intake and comparison between intake and 24-h excretion of sodium

To estimate cross-sectional and long-term dietary sodium intakes and sources in Finland, and to evaluate the validity of 48-h recall to assess sodium intake. Cross-sectional dietary surveys and food availability data (Food Balance Sheets). Dietary surveys were carried out in Finland in 1992, 1997 and 2002. Food availability data were collected from 1980 to 1999. A stratified random sample was drawn from the population register. The total number of participants in the three dietary surveys was 6730. In the subsample for urine collection, the number of participants was 879. Nutrient intakes were estimated on the basis of a 3-day food diary in 1992, a 24-h recall in 1997 and a 48-h recall in 2002. The 24-h urinary excretion of sodium was used to validate sodium intake. In addition, salt intake was estimated based on Food Balance Sheets. Sodium intake has slowly decreased since the early 1980s. Reported daily sodium intake correlated significantly with sodium excretion. Sodium intake has decreased during the last two decades, but is still higher than the recommended daily intake. Sodium intake estimation based on dietary surveys and food availability data is a valid method provided that the food composition database is up to date and of good quality. All surveys were funded by the National Public Health Institute in Finland and the Ministry of Social Affairs and Health.

Salt-The Forgotten Renal Risk Factor: Sodium Intake Affects Urinary Albumin Excretion Especially in Overweight Subjects. J Intern Med 256: 324-330, 2004.

Decades ago, following the work of Ambard and Beaujard (1), dietary sodium restriction became a mainstay of the treatment of patients with renal disease on both sides of the Atlantic, although admittedly based on very limited evidence (2,3). Subsequently, the adverse effect of salt was ascribed to hypervolemia and hypertension. After diuretics and effective antihypertensive agents had become available, dietary restriction of salt had fallen out of fashion in the perhaps premature belief that any adverse effect of salt can be prevented by augmenting natriuresis using diuretics, although at least in experimental studies this was by no means the case (4). With respect to BP and cardiovascular risk, salt has recently seen a renaissance. In the Dietary Approaches to Stop Hypertension (DASH) Study, lowering of dietary salt from usual to low intake with simultaneous further modifications of the diet decreased systolic BP by 7.1 mmHg overall and by 11.5 mmHg in hypertensive individuals (5). A meta-analysis concluded that the BP difference between intake of 12 g and 3 g of salt, i.e., sodium chloride, was 5.6/3.2 mmHg in hypertensive and 3.5/1.8 mmHg in normotensive subjects (6). In a prospective Finnish study, a 100 mmol/d difference in sodium intake was associated with a relative risk of coronary heart disease of 1.5 and of all cause mortality of 1.2, independent of BP and classic cardiovascular risk factors (7). In contrast to impressive experimental studies, for instance in intact rats and in antithymocyte serum nephritis as well as postangiotensin infusion (8–10), very little clinical information has been presented. It is therefore of considerable interest that in a cross-sectional cohort study of 7850 subjects aged 28 to 75 yr in the city of Groningen (The Netherlands), a significant positive relationship was demonstrated between dietary sodium intake and urinary albumin excretion. The association was independent of gender, age, BP, body mass index (BMI), waist-to-hip ratio, serum cholesterol, or glucose concentration. The difference between the lowest quintile of sodium excretion (mean, 70.5 mmol/d) and the highest (mean, 220 mmol/d) was 7.5 mg albumin/d (5.3 to 13.3) versus 11.1 mg albumin/d (7.3 to 21.7). It must be admitted that other indicators of food intake were also positively associated with albuminuria, but the effect of sodium intake on urinary albumin excretion was independent of such other food constituents. Of interest with respect to potential pathogenetic mechanisms is the observation that a significant interaction was noted between urinary sodium and BMI. At any given sodium intake, subjects with a higher BMI had higher urinary albumin excretion than subjects with a lower BMI. In a large cohort, this observation amplifies and extends previous observations of the Montpellier group (11). It also confirms with more reliable assessment of sodium intake the previous observations in the National Health and Nutrition Examination Survey (NHANES I) study (12). The study has the merit of putting squarely back onto the map a hotly debated issue that has caused considerable controversy in the past, i.e., sodium chloride intake in hypertensive and particularly in renal patients. It does not answer, however, which mechanism(s) account(s) for the link. One can only speculate on the basis of animal experiments. High salt has been shown to increase left ventricular mass, AT1 receptor expression, and aldosterone synthase activity in Wistar Kyoto rats despite unchanged BP and suppression of the renin system (13). In addition, salt was also shown to induce myocardial as well as renal fibrosis (14). In the aortic endothelium (15) and in glomeruli (16), high salt increases the activities of the p38 mitogen-activated protein (MAP) kinase. In the kidney, high salt intake also increases oxidative stress (8). Of particular interest is the activation of TGF-β induced by high salt (17,18). An interesting interrelation exists between nitric oxide (NO) and TGF-β: NO inhibits TGF-β (19). The high salt sensitivity of BP in patients with renal failure may be explained by the finding that the BP response to high salt is dependent on NO production (20). In humans, the increase in renal plasma flow in response to salt loading was reduced by inhibition of NO production (21), of considerable interest because the endogenous NO synthase inhibitor L-NMMA is increased very early on in renal failure (22). In summary, there is no lack of potential pathomechanisms in the kidney (18) to speculate about the interpretation of the above findings; what is lacking is strong human evidence. In a small, retrospective series, a relation between progression and salt intake was noted (23). Certainly this issue deserves more attention. In this respect, the paper by Verhave et al. (24) will hopefully serve to wake up the renal community: There may be a chance out there to improve renal outcomes (25).

Estimation of sodium intake by urinary excretion and dietary records in children and adolescents from Porto Alegre, Brazil: a comparision of two methods

Cross-sectional population-based study conducted in the city of Porto Alegre, south Brazil, to evaluate the use of 24-hour dietary records in the assessment of sodium intake. Subjects were 188 children and adolescents aged 6 to 17 years. Overnight urine was collected for all subjects, and 24-hour urine was collected for 16% of the subjects. Daily sodium intake ranged from 8.5 to 10 g. Mean amount of sodium excreted in 24-hour urine was 83% of the mean intake calculated by dietary records. The Pearson correlation coefficient between the two methods of assessment of urinary excretion of sodium was r = 0.71 (P < 0.001). However, Bland-Altman analysis revealed that the 95% limits of agreement varied widely, thus providing evidence of the large difference between the two methods. Bland-Altman analysis could be considered an important improvement over the use of correlation coefficient to evaluate the agreement between two methods. Estimation of sodium intake by means of dietary records was inaccurate when compared with urine collections (r = −0.41; P < 0.05 (24h) and r = 0.09; P = 0.175 (overnight).

Validation of a Simple Method for Assessing Sodium Intake in Dialysis Patients

It has been reported that sodium intake can be estimated in dialysis patients by the increment in the body sodium pool from the end of a dialysis session to the beginning of the following one. To verify the reliability of this method we compared the sodium intake, estimated by the interdialytic changes in plasma sodium concentration (C) and body water volume (V), to sodium removal during three consecutive sessions. For this purpose we investigated 9 nondiabetic patients, 5 females and 4 males, under chronic hemofiltration treatment. Sodium intake was estimated by the formula (C_pre V_pre) – (C_post V_post) using a flame photometer and electrical bioimpedance to determine the plasma sodium concentration and total body water, respectively. Sodium removal was calculated by the difference between sodium loss into the ultrafiltrate and sodium gain with the reinfusion fluid. The mean values of sodium intake calculated during the three intervals corresponded with the sodium losses measured during the three hemofiltration sessions in each patient (338 ± 55 vs. 329 ± 67 mEq; r = 0.92, p < 0.0001). A direct relationship was also observed between sodium intake and both interdialytic body weight increase (r = 0.89, p < 0.0001) and fluid loss during the sessions (r = 0.88, p < 0.0001). This data demonstrates that sodium intake can be properly estimated by the interdialytic changes in body water and plasma sodium concentrations. They also suggest that fluid intake may be influenced by sodium consumption and that sodium intake monitoring could be useful for the control of excessive interdialytic fluid gain.

Assessment of sodium intake by diet record and by two overnight urine collections in both African-Americans (AA) and whites (W): The treatment of mild hypertension study (TOMHS)

Assessment of sodium intake by diet record and by two overnight urine collections in both African-Americans (AA) and whites (W): The treatment of mild hypertension study (TOMHS)