High Dietary Sodium Intake Assessed by Estimated 24-h Urinary Sodium Excretion Is Associated with NAFLD and Hepatic Fibrosis.
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ABSTRACT: Background
Although high sodium intake is associated with obesity and hypertension, few studies have investigated the relationship between sodium intake and non-alcoholic fatty liver disease (NAFLD). We evaluated the association between sodium intake assessed by estimated 24-h urinary sodium excretion and NAFLD in healthy Koreans.Methods
We analyzed data from 27,433 participants in the Korea National Health and Nutrition Examination Surveys (2008-2010). The total amount of sodium excretion in 24-h urine was estimated using Tanaka's equations from spot urine specimens. Subjects were defined as having NAFLD when they had high scores in previously validated NAFLD prediction models such as the hepatic steatosis index (HSI) and fatty liver index (FLI). BARD scores and FIB-4 were used to define advanced fibrosis in subjects with NAFLD.Results
The participants were classified into three groups according to estimated 24-h urinary excretion tertiles. The prevalence of NAFLD as assessed by both FLI and HSI was significantly higher in the highest estimated 24-h urinary sodium excretion tertile group. Even after adjustment for confounding factors including body fat and hypertension, the association between higher estimated 24-h urinary sodium excretion and NAFLD remained significant (Odds ratios (OR) 1.39, 95% confidence interval (CI) 1.26-1.55, in HSI; OR 1.75, CI 1.39-2.20, in FLI, both P < 0.001). Further, subjects with hepatic fibrosis as assessed by BARD score and FIB-4 in NAFLD patients had higher estimated 24-h urinary sodium values.Conclusions
High sodium intake was independently associated with an increased risk of NAFLD and advanced liver fibrosis.
SUBMITTER: Huh JH
PROVIDER: S-EPMC4646649 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:ImportanceIn 2010, the Institute of Medicine (now the National Academy of Medicine) recommended collecting 24-hour urine to estimate US sodium intake because previous studies indicated 90% of sodium consumed was excreted in urine.ObjectiveTo estimate mean population sodium intake and describe urinary potassium excretion among US adults.Design, setting, and participantsIn a nationally representative cross-sectional survey of the US noninstitutionalized population, 827 of 1103 (75%) randomly selected, nonpregnant participants aged 20 to 69 years in the examination component of the National Health and Nutrition Examination Survey (NHANES) collected at least one 24-hour urine specimen in 2014. The overall survey response rate for the 24-hour urine collection was approximately 50% (75% [24-hour urine component response rate] × 66% [examination component response rate]).Exposures24-hour collection of urine.Main outcomes and measuresMean 24-hour urinary sodium and potassium excretion. Weighted national estimates of demographic and health characteristics and mean electrolyte excretion accounting for the complex survey design, selection probabilities, and nonresponse.ResultsThe study sample (n = 827) represented a population of whom 48.8% were men; 63.7% were non-Hispanic white, 15.8% Hispanic, 11.9% non-Hispanic black, and 5.6% non-Hispanic Asian; 43.5% had hypertension (according to 2017 hypertension guidelines); and 10.0% reported a diagnosis of diabetes. Overall mean 24-hour urinary sodium excretion was 3608 mg (95% CI, 3414-3803). The overall median was 3320 mg (interquartile range, 2308-4524). In secondary analyses by sex, mean sodium excretion was 4205 mg (95% CI, 3959-4452) in men (n = 421) and 3039 mg (95% CI, 2844-3234) in women (n = 406). By age group, mean sodium excretion was 3699 mg (95% CI, 3449-3949) in adults aged 20 to 44 years (n = 432) and 3507 mg (95% CI, 3266-3748) in adults aged 45 to 69 years (n = 395). Overall mean 24-hour urinary potassium excretion was 2155 mg (95% CI, 2030-2280); by sex, 2399 mg (95% CI, 2253-2545) in men and 1922 mg (95% CI, 1757-2086) in women; and by age, 1986 mg (95% CI, 1878-2094) in adults aged 20 to 44 years and 2343 mg (95% CI, 2151-2534) in adults aged 45 to 69 years.Conclusions and relevanceIn cross-sectional data from a 2014 sample of US adults, estimated mean sodium intake was 3608 mg per day. The findings provide a benchmark for future studies.
| S-EPMC5885845 | biostudies-literature
Project description:ObjectiveThe gold standard method for measuring population sodium intake is based on a 24 h urine collection carried out in a random population sample. However, because participant burden is high, response rates are typically low with less than one in four agreeing to provide specimens. At this low level of response it is possible that simply asking for volunteers would produce the same results.SettingLithgow, New South Wales, Australia.ParticipantsWe randomly selected 2152 adults and obtained usable 24 h urine samples from 306 (response rate 16%). Specimens were also collected from a further 113 volunteers. Estimated salt consumption and the costs for each strategy were compared.ResultsThe characteristics of the 'random' and 'volunteer' samples were moderately different in mean age 58 (SD 14.6 vs 49(17.7) years, respectively; p<0.001) as well as self-reported alcohol use, tobacco use, history of hypertension and prescription drug use (all p<0.04). Overall crude mean 24 h urinary salt excretion was 8.9(3.6) g/day in the random sample vs 8.5(3.3) g/day for the volunteers (p=0.42). Corresponding age-adjusted and sex-adjusted estimates were 9.2(3.3) and 8.8(3.4) g/day (p=0.29). Estimates for men 10.3(3.8) vs 9.6(3.3) g/day; (p=0.26) and women 7.6(3) vs 7.9(3.2) g/day; (p=0.43) were also similar for the two samples, as was salt excretion across age groups (p=0.72). The cost of obtaining each 24 h urine sample was two times greater for the random compared to volunteer samples ($A62 vs $A31).ConclusionsThe estimated salt consumption derived from the two samples was comparable and was not substantively different to estimates obtained from other surveys. In countries where salt is pervasive and cannot easily be avoided, estimates of consumption obtained from volunteer samples may be valid and less costly.
| S-EPMC3902305 | biostudies-literature
Project description:The association between sodium intake and long-term kidney disease endpoints is debated and yet to be proven. We aimed to investigate the associations of estimated 24-h urinary sodium excretion, reflecting daily sodium intake, with the incidence of end-stage kidney disease (ESKD). In this prospective cohort study including 444,375 UK Biobank participant, 865 (0.2%) ESKD events occurred after median follow-up of 12.7 years. For every 1 g increment in estimated 24-h urinary sodium excretion, multivariable-adjusted hazard ratio for incident ESKD was 1.09 (95% confidence interval 0.94-1.26). Nonlinear associations were not detected with restricted cubic splines. The null findings were confirmed by a series of sensitivity analyses, which attenuated potential bias from measurement errors of the exposure, regression dilution, reverse causality, and competing risks. In conclusion, there is insufficient evidence that estimated 24-h urinary sodium excretion is associated with the incidence of ESKD.
| S-EPMC10192648 | biostudies-literature
Project description:A higher sodium intake is conceivably associated with insulin resistant conditions like obesity, but associations of non-alcoholic fatty liver disease (NAFLD) with a higher sodium intake determined by 24 hours (24 h) urine collections are still unclear. Dietary sodium intake was measured by sodium excretion in two complete consecutive 24 h urine collections in 6132 participants of the Prevention of Renal and Vascular End-Stage Disease (PREVEND) cohort. Fatty Liver Index (FLI) ≥60 and Hepatic Steatosis Index (HSI) >36 were used as proxies of suspected NAFLD. 1936 (31.6%) participants had an FLI ≥60, coinciding with the increased prevalence of type 2 diabetes (T2D), metabolic syndrome, hypertension and history of cardiovascular disease. Sodium intake was higher in participants with an FLI ≥60 (163.63 ± 61.81 mmol/24 h vs. 136.76 ± 50.90 mmol/24 h, p < 0.001), with increasing incidence in ascending quartile categories of sodium intake (p < 0.001). Multivariably, an FLI ≥60 was positively associated with a higher sodium intake when taking account for T2D, a positive cardiovascular history, hypertension, alcohol intake, smoking and medication use (odds ratio (OR) 1.54, 95% confidence interval (CI) 1.44-1.64, p < 0.001). Additional adjustment for the Homeostasis Model Assessment of Insulin Resistance (HOMA-IR) diminished this association (OR 1.30, 95% CI 1.21-1.41, p < 0.001). HSI >36 showed similar results. Associations remained essentially unaltered after adjustment for body surface area or waist/hip ratio. In conclusion, suspected NAFLD is a feature of higher sodium intake. Insulin resistance-related processes may contribute to the association of NAFLD with sodium intake.
| S-EPMC6947413 | biostudies-literature
Project description:Epidemiological studies of the association of sodium and potassium intake with cardiovascular disease risk have almost exclusively relied on self-reported dietary data. Here, 24-hour urinary excretion assessments are used to correct the dietary self-report data for measurement error under the assumption that 24-hour urine recovery provides a biomarker that differs from usual intake according to a classical measurement model. Under this assumption, dietary self-reports underestimate sodium by 0% to 15%, overestimate potassium by 8% to 15%, and underestimate sodium/potassium ratio by ≈20% using food frequency questionnaires, 4-day food records, or three 24-hour dietary recalls in Women's Health Initiative studies. Calibration equations are developed by linear regression of log-transformed 24-hour urine assessments on corresponding log-transformed self-report assessments and several study subject characteristics. For each self-report method, the calibration equations turned out to depend on race and age and strongly on body mass index. After adjustment for temporal variation, calibration equations using food records or recalls explained 45% to 50% of the variation in (log-transformed) 24-hour urine assessments for sodium, 60% to 70% of the variation for potassium, and 55% to 60% of the variation for sodium/potassium ratio. These equations may be suitable for use in epidemiological disease association studies among postmenopausal women. The corresponding signals from food frequency questionnaire data were weak, but calibration equations for the ratios of sodium and potassium/total energy explained ≈35%, 50%, and 45% of log-biomarker variation for sodium, potassium, and their ratio, respectively, after the adjustment for temporal biomarker variation and may be suitable for cautious use in epidemiological studies. Clinical Trial Registration- URL: www.clinicaltrials.gov. Unique identifier: NCT00000611.
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Project description:Background/aimsWe explored whether high sodium intake, assessed by urinary excretion, determines the risk of sarcopenia and nonalcoholic fatty liver disease (NAFLD).MethodsWe analyzed 10,036 adult participants with normal kidney function from the Korea National Health and Nutrition Examination Survey (2008-2011). NAFLD was identified using the fatty liver index, and the muscle mass was evaluated using dual X-ray absorptiometry. The dietary sodium intake was estimated using Tanaka's equation.ResultsThe mean 24-hour urinary sodium excretion was 144.2±36.1 mmol/day (corresponding to 3.3 g/day Na) in the total population. The 24-hour urinary sodium excretion showed moderate accuracy in predicting NAFLD (area under the receiver operating characteristic, 0.702; 95% confidence interval [CI], 0.692 to 0.712). A cutoff value of 99.96 mmol/day (corresponding to 2.30 g/day Na) for urinary sodium excretion in predicting NAFLD showed 76.1% sensitivity and 56.1% specificity. The results of multiple adjusted models indicated that the participants with the highest urinary sodium excretion had a significantly higher risk of NAFLD (odds ratio, 1.46; 95% CI, 1.27 to 1.66; p<0.001) and sarcopenia (odds ratio, 1.49; 95% CI, 1.28 to 1.73; p<0.001) than those with the lowest urinary sodium excretion. The association between a higher 24-hour urinary sodium excretion and NAFLD was independent of sarcopenia.ConclusionsParticipants with a high sodium intake, as assessed by sodium excretion, had a substantial risk of NAFLD and sarcopenia.
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Project description:BackgroundThe relation between sodium intake and cardiovascular disease remains controversial, owing in part to inaccurate assessment of sodium intake. Assessing 24-hour urinary excretion over a period of multiple days is considered to be an accurate method.MethodsWe included individual-participant data from six prospective cohorts of generally healthy adults; sodium and potassium excretion was assessed with the use of at least two 24-hour urine samples per participant. The primary outcome was a cardiovascular event (coronary revascularization or fatal or nonfatal myocardial infarction or stroke). We analyzed each cohort using consistent methods and combined the results using a random-effects meta-analysis.ResultsAmong 10,709 participants, who had a mean (±SD) age of 51.5±12.6 years and of whom 54.2% were women, 571 cardiovascular events were ascertained during a median study follow-up of 8.8 years (incidence rate, 5.9 per 1000 person-years). The median 24-hour urinary sodium excretion was 3270 mg (10th to 90th percentile, 2099 to 4899). Higher sodium excretion, lower potassium excretion, and a higher sodium-to-potassium ratio were all associated with a higher cardiovascular risk in analyses that were controlled for confounding factors (P≤0.005 for all comparisons). In analyses that compared quartile 4 of the urinary biomarker (highest) with quartile 1 (lowest), the hazard ratios were 1.60 (95% confidence interval [CI], 1.19 to 2.14) for sodium excretion, 0.69 (95% CI, 0.51 to 0.91) for potassium excretion, and 1.62 (95% CI, 1.25 to 2.10) for the sodium-to-potassium ratio. Each daily increment of 1000 mg in sodium excretion was associated with an 18% increase in cardiovascular risk (hazard ratio, 1.18; 95% CI, 1.08 to 1.29), and each daily increment of 1000 mg in potassium excretion was associated with an 18% decrease in risk (hazard ratio, 0.82; 95% CI, 0.72 to 0.94).ConclusionsHigher sodium and lower potassium intakes, as measured in multiple 24-hour urine samples, were associated in a dose-response manner with a higher cardiovascular risk. These findings may support reducing sodium intake and increasing potassium intake from current levels. (Funded by the American Heart Association and the National Institutes of Health.).
| S-EPMC9153854 | biostudies-literature
Project description:AimsThe objective was to evaluate whether sodium intake, assessed with the gold standard 24-h urinary collections, was related to long-term incidence of death, cardiovascular disease (CVD) and diabetes mellitus (DM).MethodsA cohort of 4630 individuals aged 25-64 years collected 24-h urine samples in 1979-2002 and were followed up to 14 years for the incidence of any CVD, coronary heart disease (CHD), stroke, heart failure (HF) and DM event, and death. Cox proportional hazards models were used to estimate the association between the baseline salt intake and incident events and adjusted for baseline age, body mass index, serum cholesterol, prevalent DM, and stratified by sex and cohort baseline year.ResultsDuring the follow-up, we observed 423 deaths, 424 CVD events (288 CHD events, 142 strokes, 139 HF events) and 161 DM events. Compared with the highest quartile of salt intake, persons in the lowest quartile had a lower incidence of CVD (hazard ratio [HR] 0.70; 95% confidence interval [CI], 0.51-0.95, p = .02), CHD (HR 0.63 [95% CI 0.42-0.94], p = .02) and DM (HR 0.52 [95% CI 0.31-0.87], p = .01). The results were non-significant for mortality, HF, and stroke.ConclusionHigh sodium intake is associated with an increased incidence of CVD and DM.
| S-EPMC7877963 | biostudies-literature
Project description:The present study evaluated the reliability of equations using spot urine (SU) samples in the estimation of 24-hour urine sodium excretion (24-HUNa). Equations estimating 24-HUNa from SU samples were derived from first-morning SU of 101 participants (52.4 ± 11.1 years, range 24-70 years). Equations developed by us and other investigators were validated with SU samples from a separate group of participants (n = 224, 51.0 ± 10.9 years, range 24-70 years). Linear, quadratic, and cubic equations were derived from first-morning SU samples because these samples had a sodium/creatinine ratio having the highest correlation coefficient for 24-HUNa/creatinine ratio (r = 0.728, p < 0.001). In the validation group, the estimated 24-HUNa showed significant correlations with measured 24-HUNa values. The estimated 24-HUNa by the linear, quadratic, and cubic equations developed from our study were not significantly different from measured 24-HUNa, while estimated 24-HUNa by previously developed equations were significantly different from measured 24-HUNa values. The limits of agreement between measured and estimated 24-HUNa by six equations exceeded 100 mmol/24-hour in the Bland-Altman analysis. All equations showed a tendency of under- or over-estimation of 24-HUNa, depending on the level of measured 24-HUNa. Estimation of 24-HUNa from single SU by equations as tested in the present study was found to be inadequate for the estimation of an individual's 24-HUNa.
| S-EPMC4073156 | biostudies-literature
Project description:High intakes of dietary sodium are associated with elevated blood pressure levels and an increased risk of cardiovascular disease. National and international guidelines recommend reduced sodium intake in the general population, which necessitates population-wide surveillance. We assessed the utility of casual (spot) urine specimens in estimating 24-hour urinary sodium excretion as a marker of sodium intake in the International Cooperative Study on Salt, Other Factors, and Blood Pressure. There were 5,693 participants recruited in 1984-1987 at the ages of 20-59 years from 29 North American and European samples. Participants were randomly assigned to test or validation data sets. Equations derived from casual urinary sodium concentration and other variables in the test data were applied to the validation data set. Correlations between observed and estimated 24-hour sodium excretion were 0.50 for individual men and 0.51 for individual women; the values were 0.79 and 0.71, respectively, for population samples. Bias in mean values (observed minus estimated) was small; for men and women, the values were -1.6 mmol per 24 hours and 2.3 mmol per 24 hours, respectively, at the individual level and -1.8 mmol per 24 hours and 2.2 mmol per 24 hours, respectively, at the population level. Proportions of individuals with urinary 24-hour sodium excretion above the recommended levels were slightly overestimated by the models. Casual urine specimens may be a useful, low-burden, low-cost alternative to 24-hour urine collections for estimation of population sodium intakes; ongoing calibration with study-specific 24-hour urinary collections is recommended to increase validity.
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