Estimating 24-Hour Sodium Excretion from Spot Urine Samples in Chinese Adults: Can Spot Urine Substitute 24-Hour Urine Samples?

Several estimating equations for predicting 24-h urinary sodium (24-hUNa) excretion using spot urine (SU) samples have been developed, but have not been readily available to Chinese populations. We aimed to compare and validate the six existing methods at population level and individual level. We extracted 1671 adults eligible for both 24-h urine and SU sample collection. Mean biases (95% CI) of predicting 24-hUNa excretion using six formulas were 58.6 (54.7, 62.5) mmol for Kawasaki, -2.7 (-6.2, 0.9) mmol for Tanaka, -24.5 (-28.0, -21.0) mmol for the International Cooperative Study on Salt, Other Factors, and Blood Pressure (INTERSALT) with potassium, -26.8 (-30.1, -23.3) mmol for INTERSALT without potassium, 5.9 (2.3, 9.6) mmol for Toft, and -24.2 (-27.7, -20.6) mmol for Whitton. The proportions of relative difference >40% with the six methods were nearly a third, and the proportions of absolute difference >51.3 mmol/24-h (3 g/day salt) were more than 40%. The misclassification rate were all >55% for the six methods at the individual level. Although the Tanaka method could offer a plausible estimation for surveillance of the population sodium excretion in Shandong province, caution remains when using the Tanaka formula for other provincial populations in China. However, these predictive methods were inadequate to evaluate individual sodium excretion.

Dietary Intake and Sources of Potassium in a Cross-Sectional Study of Australian Adults.

A diet rich in potassium is important to reduce the risk of cardiovascular disease. This study assessed potassium intake; food sources of potassium (including NOVA level of processing, purchase origin of these foods); and sodium-to-potassium ratio (Na:K) in a cross-section of Australian adults. Data collection included 24-h urines (n = 338) and a 24-h diet recall (subsample n = 142). The mean (SD) age of participants was 41.2 (13.9) years and 56% were females. Mean potassium (95%CI) 24-h urinary excretion was 76.8 (73.0-80.5) mmol/day compared to 92.9 (86.6-99.1) by 24-h diet recall. Na:K was 1.9 (1.8-2.0) from the urine excretion and 1.4 (1.2-1.7) from diet recall. Foods contributing most to potassium were potatoes (8%), dairy milk (6%), dishes where cereal is the main ingredient (6%) and coffee/coffee substitutes (5%). Over half of potassium (56%) came from minimally processed foods, with 22% from processed and 22% from ultraprocessed foods. Almost two-thirds of potassium consumed was from foods purchased from food stores (58%), then food service sector (15%), and fresh food markets (13%). Overall, potassium levels were lower than recommended to reduce chronic disease risk. Multifaceted efforts are required for population-wide intervention-aimed at increasing fruit, vegetable, and other key sources of potassium intake; reducing consumption of processed foods; and working in supermarket/food service sector settings to improve the healthiness of foods available.

Trend of salt intake measured by 24-hour urine collection samples among Iranian adults population between 1998 and 2013: The Isfahan salt study.

BACKGROUND AND AIM: Few population-based studies conducted in the Eastern Mediterranean region assessed salt intake by the measurement of 24-h sodium urine excretion (24-hUNa). The current study aimed to assess the trend of mean salt intake in Iranian adults between 1998 and 2013. METHODS AND RESULTS: These cross-sectional studies were performed on 564, 157, 509 and 837 randomly selected healthy adults aged >18 years from Isfahan city, Iran, in 1998, 2001, 2007 and 2013, respectively. BP was measured using a mercury sphygmomanometer according to a standard protocol. Single 24-h urine was collected to assess 24-hUNa as a surrogate of salt intake, and 24-h urinary K (24-hUK). The estimated trend of salt intake was 9.5, 9.7, 9.6 and 10.2 g/day in total population (P < 0.001). The increase in salt intake between 1998 and 2013 was significant only in men, (P < 0.001). The risk of pre-hypertension was 21% and 18% significantly greater in the highest quartiles of UNa/UK after adjustment for potential confounders in 2001 and 2013, respectively, [OR (95% CI): 1.21 (1.03-1.64) and 1.18 (1.02-1.38), respectively]. CONCLUSIONS: This population-based study indicated that mean salt intake was about two times of recommendation in Isfahan city, Iran, and suggest that it would be essential to implement a salt reduction strategy program in Iranian population. Longitudinal national studies with larger samples examining the trend of salt intake are warranted.

Associations of Usual 24-Hour Sodium and Potassium Intakes with Blood Pressure and Risk of Hypertension among Adults in China's Shandong and Jiangsu Provinces.

BACKGROUND/AIMS: High sodium intake and low intake of potassium can increase blood pressure (BP) and risk of developing hypertension. Few studies have examined the association between 24-h urinary sodium and potassium excretion and BP or risk of hypertension in China, and most used only a single 24-h urinary sample. METHODS: We analyzed data on 2281 participants aged 18-69 years by using two 24-h urinary sodium and potassium excretions from the supplemental baseline survey of the Shandong-Ministry of Health Action on Salt Reduction and Hypertension (SMASH) project. We used measurement error models to estimate usual intakes, multivariable linear regression to assess their association with B P, and logistic regression to estimate the risk of hypertension. RESULTS: The average usual intakes of sodium and potassium, and the mean sodium-potassium ratio, were 166.9 mmol/day, 25.3 mmol/day, and 6.8, respectively. All three measures were significantly associated with systolic BP (SBP) and diastolic BP (DBP), with an increase of 1.39 mmHg (95% confidence interval [CI] 0.44─2.34) in SBP and 0.94 mmHg (95% CI 0.34─1.55) in DBP for a 1-standard deviation (SD) (25.6mmol/day) increase in sodium intake, a decrease of 1.42 mmHg (95% CI -2.37─ -0.47) in SBP and 0.91 mmHg (95% CI -1.52─ -0.30) in DBP for a 1-SD (3.4 mmol/day) increase in potassium intake, and an increase of 0.97 mmHg (95% CI 0.36─1.58) in SBP and of 0.65 mmHg (95% CI 0.26─1.04) in DBP per unit increase in the sodium-to-potassium ratio. The adjusted odds ratios comparing the risk of hypertension among adults in the highest with those in the lowest quintile differ significantly for potassium (0.51; 95% CI 0.29─0.88) and sodium-to-potassium ratio (1.40; 95% CI 1.01─1.94). CONCLUSIONS: Our results suggested that higher sodium and lower potassium intakes are associated with increased BP and risk of hypertension in the Shandong and Jiangsu adults.

Applying recovery biomarkers to calibrate self-report measures of sodium and potassium in the Hispanic Community Health Study/Study of Latinos.

Measurement error in assessment of sodium and potassium intake obscures associations with health outcomes. The level of this error in a diverse US Hispanic/Latino population is unknown. We investigated the measurement error in self-reported dietary intake of sodium and potassium and examined differences by background (Central American, Cuban, Dominican, Mexican, Puerto Rican and South American). In 2010-2012, we studied 447 participants aged 18-74 years from four communities (Miami, Bronx, Chicago and San Diego), obtaining objective 24-h urinary sodium and potassium excretion measures. Self-report was captured from two interviewer-administered 24-h dietary recalls. Twenty percent of the sample repeated the study. We examined bias in self-reported sodium and potassium from diet and the association of mismeasurement with participant characteristics. Linear regression relating self-report with objective measures was used to develop calibration equations. Self-report underestimated sodium intake by 19.8% and 20.8% and potassium intake by 1.3% and 4.6% in men and women, respectively. Sodium intake underestimation varied by Hispanic/Latino background (P<0.05) and was associated with higher body mass index (BMI). Potassium intake underestimation was associated with higher BMI, lower restaurant score (indicating lower consumption of foods prepared away from home and/or eaten outside the home) and supplement use. The R2 was 19.7% and 25.0% for the sodium and potassium calibration models, respectively, increasing to 59.5 and 61.7% after adjusting for within-person variability in each biomarker. These calibration equations, corrected for subject-specific reporting error, have the potential to reduce bias in diet-disease associations within this largest cohort of Hispanics in the United States.

Effects of sodium and potassium supplementation on endothelial function: a fully controlled dietary intervention study.

High Na and low K intakes have adverse effects on blood pressure, which increases the risk for CVD. The role of endothelial dysfunction and inflammation in this pathophysiological process is not yet clear. In a randomised placebo-controlled cross-over study in untreated (pre)hypertensives, we examined the effects of Na and K supplementation on endothelial function and inflammation. During the study period, subjects were provided with a diet that contained 2·4 g/d of Na and 2·3 g/d of K for a 10 460 kJ (2500 kcal) intake. After 1-week run-in, subjects received capsules with supplemental Na (3·0 g/d), supplemental K (2·8 g/d) or placebo, for 4 weeks each, in random order. After each intervention, circulating biomarkers of endothelial function and inflammation were measured. Brachial artery flow-mediated dilation (FMD) and skin microvascular vasomotion were assessed in sub-groups of twenty-two to twenty-four subjects. Of thirty-seven randomised subjects, thirty-six completed the study. Following Na supplementation, serum endothelin-1 was increased by 0·24 pg/ml (95 % CI 0·03, 0·45), but no change was seen in other endothelial or inflammatory biomarkers. FMD and microvascular vasomotion were unaffected by Na supplementation. K supplementation reduced IL-8 levels by 0·28 pg/ml (95 % CI 0·03, 0·53), without affecting other circulating biomarkers. FMD was 1·16 % (95% CI 0·37, 1·96) higher after K supplementation than after placebo. Microvascular vasomotion was unaffected. In conclusion, a 4-week increase in Na intake increased endothelin-1, but had no effect on other endothelial or inflammatory markers. Increased K intake had a beneficial effect on FMD and possibly IL-8, without affecting other circulating endothelial or inflammatory biomarkers.

Effects of a high salt intake and potassium supplementation on QT interval dispersion in normotensive healthy subjects.

OBJECTIVE: To evaluate the effects of dietary sodium intake on QT interval dispersion (QTd) in normotensive healthy subjects and assess the protective effects of dietary potassium. Methods All subjects were sequentially maintained on a protocol with a three-day baseline investigation, seven-day low-salt period (3 g/day (d), NaCL), seven-day salt loading period (18 g/d, NaCL) and a seven-day salt loading with potassium supplementation period (4.5 g/d, KCL). On the last day of each period, 24-hour urine samples were collected, the blood pressure values were measured and an electrocardiogram was recorded. The QT interval, QTd and T peak-T end interval (Tp-Te) were subsequently measured and calculated. Patients Sixty-four normotensive subjects, men and women, ranging from 28 to 60 years of age, were enrolled. Results There were no great fluctuations in heart rate after salt loading, whereas the systolic blood pressure (SBP, mmHg) and diastolic blood pressure (DBP, mmHg) increased and the corrected QT interval (QTc), corrected QT interval dispersion (QTdc) and Tp-Te values were significantly prolonged compared to that observed in the low-salt period (SBP, 118.6 ± 13.5 vs. 111.7 ± 11.3, p<0.01; DBP, 76.9 ± 8.6 vs. 71.7 ± 7.7, p<0.01; QTdc, 60.3 ± 19.4 vs. 55.6 ± 19.4, p<0.05; Tp-Te, 83.0 ± 10.1 vs. 79.8 ± 8.5, p<0.01). Surprisingly, all of these changes were reversed by potassium supplementation (SBP, 114.5 ± 12.3 vs.118.6 ± 13.5, p<0.01; DBP, 72.2 ± 7.9 vs.76.9 ± 8.6, p<0.01;QTd, 42.6 ± 15.1 vs. 47.4 ± 19.0, p<0.05; QTdc, 52.2 ± 18.0 vs. 60.3 ± 19.4, p<0.05; Tp-Te, 79.1 ± 8.5 vs. 83.0 ± 10.1, p<0.01). Conclusion Salt loading prolongs the QT interval, QTd and Tp-Te, while dietary potassium supplementation reverses these alterations. These findings suggest that potassium supplementation may improve variation in the healing time and prevent arrhythmia.

LCZ696, Angiotensin II Receptor-Neprilysin Inhibitor, Ameliorates High-Salt-Induced Hypertension and Cardiovascular Injury More Than Valsartan Alone.

BACKGROUND: LCZ696, an angiotensin receptor-neprilysin inhibitor, has recently been demonstrated to exert more beneficial effects on hypertensive or heart failure patients than conventional renin-angiotensin system blockers. However, the mechanism underlying the benefit of LCZ696 remains to be understood. The present study was undertaken to examine the effect of LCZ696 compared with valsartan on hypertension and cardiovascular injury. METHODS: (i) Using telemetry, we compared the hypotensive effect of LCZ696 and valsartan in spontaneously hypertensive rats (SHR) that were fed a high-salt diet followed by a low-salt diet. (ii) We also examined the comparative effect of LCZ696 and valsartan on salt loaded SHRcp, a model of metabolic syndrome. RESULTS: (i) LCZ696 exerted a greater blood pressure (BP) lowering effect than valsartan in SHR regardless of high-salt or low-salt intake. Additive BP reduction by LCZ696 was associated with a significant increase in urinary sodium excretion and sympathetic activity suppression. (ii) LCZ696 significantly ameliorated cardiac hypertrophy and inflammation, coronary arterial remodeling, and vascular endothelial dysfunction in high-salt loaded SHRcp compared with valsartan. CONCLUSIONS: LCZ696 caused greater BP reduction than valsartan in SHR regardless of the degree of salt intake, which was associated with a significant enhancement in urinary sodium excretion and sympathetic activity suppression. Furthermore, an additive BP lowering effect of LCZ696 led to greater cardiovascular protection in hypertensive rats.

Reproducibility of blood pressure responses to dietary sodium and potassium interventions: the GenSalt study.

Blood pressure responses to dietary sodium and potassium interventions vary among individuals. We studied the long-term reproducibility of blood pressure responses to dietary sodium and potassium intake. We repeated the dietary sodium and potassium interventions among 487 Chinese adults 4.5 years after the original dietary intervention. The identical dietary intervention protocol, which included a 7-day low-sodium feeding (51.3 mmol/d), a 7-day high-sodium feeding (307.8 mmol/d), and a 7-day high-sodium feeding with oral potassium supplementation (60.0 mmol/d), was applied in both the initial and repeated studies. Three blood pressure measurements were obtained during each of the 3 days of baseline observation and on days 5, 6, and 7 of each intervention period. The results from the 24-hour urinary excretion of sodium and potassium showed excellent compliance with the study diet. Blood pressure responses to dietary intervention in the original and repeated studies were highly correlated. For example, the correlation coefficients (95% confidence interval) for systolic blood pressure levels were 0.77 (0.73-0.80) at baseline, 0.79 (0.75-0.82) during low sodium, 0.80 (0.77-0.83) during high sodium, and 0.82 (0.79-0.85) during high sodium and potassium supplementation interventions (all P<0.0001). The correlation coefficients for systolic blood pressure changes were 0.37 (0.29-0.44) from baseline to low sodium, 0.37 (0.29-0.44) from low to high sodium, and 0.28 (0.20-0.36) from high sodium to high sodium plus potassium supplementation (all P<0.0001). These data indicate that blood pressure responses to dietary sodium and potassium interventions have long-term reproducibility and stable characteristics in the general population.

The effects of high-impact and resistance exercise on urinary calcium excretion.

Although physical activity is known to improve bone mineralization, it is unclear whether this occurs through altered absorption and/or excretion. The purpose of this study was to investigate the effects of a high-impact and resistance-training exercise program versus a period of restricted physical activity on urinary calcium excretion. Ten healthy, moderately active men (27.0 +/- 5.8 yr) participated in a 3-wk randomized crossover study. Participants were assigned to complete either a period of daily participation in exercise including high-impact and resistance-training activities (EX) or a period of restriction in physical activity (NE) for 7 consecutive days. After a 1-wk washout period, participants completed the opposite trial. During both phases, participants consumed four 8-oz servings of low-fat (1%) milk daily and avoided other dietary and supplemental sources of calcium. Urine was collected throughout the final 72 hr of each study phase. Urinary calcium and sodium excretions were 14.7% +/- 17.1% and 15.8% +/- 9.9% lower (p < .05), respectively, during the EX phase than the NE phase. These results occurred despite participants consuming more (p < .05) sodium during the EX phase than the NE phase. These results suggest that healthy, moderately active men excrete significantly less urinary calcium concurrent with lower sodium excretion during a week of performing high-impact and resistance-training exercises versus a week of restricted physical activity. The reduction in urinary loss of calcium might be at least partially responsible for improved bone mineralization that has been observed during periods of greater physical activity.

Food mineral composition and acid-base balance in preterm infants.

BACKGROUND: Due to a transient age-related low renal capacity for net acid excretion, preterm infants fed formula are at a considerable risk of spontaneously developing incipient late metabolic acidosis, clinically characterized by e.g., disturbed bone mineralization and impaired growth. AIM OF THE STUDY: From acid-base data in blood and urine under different diets of modified human milk or preterm formulas is attempted to explore the impact of food mineral (and protein) composition on renal regulation and systemic acid-base balance in preterm infants. PATIENTS AND METHODS: Data were collected from 48 infants fed their own mother's milk (28 native human milk, 20 enriched with fortifier) and 34 patients on formula (23 on a standard batch, 11 on a modified batch with reduced acid load). Intake of food was measured and acid-base data were determined in blood and timed-urine (8-12 h) samples. RESULTS: Differences in mineral composition of the diets led to considerable differences of daily "alkali-intake", without significant effects on non-respiratory (base excess, BE) and respiratory (PCO(2)) acid-base data in the blood. In contrast, a highly significant proportionality between individual dietary alkali intake and daily renal base (Na(+) + K(+)-Cl(-)) excretion was observed (y = 0.32x-0.70, n = 80, r = 0.77, P < 0.0001), irrespective of the type of the diet. CONCLUSION: Renal base saving mechanisms are normally effective in preterm infants to compensate for differences in dietary acid-base load. Generally, nutritional acid-base challenges can be judged much earlier and more safely by urinary than by blood acid-base analysis. Taking into account the age specific low capacity for renal NAE, the relatively high nutritional acid load of preterm standard formula should be reduced.

Does dietary recall adequately assess sodium, potassium, and calcium intake in hypertensive patients?

OBJECTIVE: A diet low in sodium, high in potassium, and high in calcium is recommended to lower blood pressure. However, compliance with this diet is poor, probably because of dietary intake underestimation. Therefore, we compared electrolyte intake as estimated from dietary recall with a 24-h urinary excretion. METHODS: Thirty-six patients (26 men and 10 women) with a mean age of 46 +/- 8 y participated in the study. All participants had essential hypertension and were on no drug therapy (n = 20) or non-diuretic monotherapy (n = 16). Patients were instructed to consume a low-sodium (50 mmol/d), high-potassium (supplementation with 30 to 60 mmol/d), and high-calcium (1000 mg/d) diet. Compliance with the diet was assessed at baseline and then 1, 2, and 3 mo after starting the diet. Sodium, potassium, and calcium intakes were carefully estimated from patients' dietary recall and 24-h urinary collection. RESULTS: Estimated sodium intake significantly correlated with 24-h urinary excretion (R = 0.43 P < 0.001). However, estimated sodium intake was lower than urinary sodium excretion by 34% at baseline and by 47% after 3 mo of dieting (P < 0.05). Estimated potassium intake correlated with 24-h urinary excretion. Estimated calcium intake significantly increased from 933 +/- 83 mg/d to 1029 +/- 171 mg/d (P < 0.05). Calcium intake derived from patients' recall far exceeded and only slightly correlated with 24-h urinary excretion (R = 0.23, P < 0.01). CONCLUSIONS: Patients tend to underestimate their sodium intake by 30% to 50%; therefore, urinary sodium excretion is more accurate to assess sodium intake. Thus, 24-h urinary sodium excretion should be used in clinical practice and in clinical trials, especially when dietary non-compliance is suspected.

Diet enrichment with calcium and magnesium enhances the cholesterol-lowering effect of plant sterols in obese Zucker rats.

BACKGROUND AND AIM: Recent clinical studies have demonstrated that plant sterols moderately lower serum cholesterol levels in patients with mild hypercholesterolemia. Furthermore, there is evidence suggesting that mineral nutrients, such as calcium and magnesium, may also decrease serum cholesterol concentrations. In this study, we tested the hypothesis that supplementation with mineral nutrients may enhance the cholesterol-lowering effect of plant sterols in obese Zucker rats. Furthermore, we compared the lipid-lowering effects of monovalent sodium and potassium cations with those of divalent calcium and magnesium cations. METHODS AND RESULTS: A Western-type high-fat/high-cholesterol diet increased serum cholesterol by 175% and liver cholesterol by 65% in comparison with a low-fat/low-cholesterol control diet. On the contrary, the high-fat/high-cholesterol diet decreased intestinal cholesterol absorption, as assessed by means of serum campesterol-, sitosterol-, and sitostanol-to-cholesterol ratios, thus indicating that it was under negative feedback regulation. Supplementation of the high-fat/high-cholesterol diet with plant sterols or mineral nutrients partially prevented the diet-induced increased in serum cholesterol and, when given concurrently, their cholesterol-lowering effect was enhanced. Their combination also effectively prevented the diet-induced increase in liver cholesterol concentration, and had beneficial effects on liver and myocardial hypertrophy, and the development of obesity. These beneficial effects were at least partially mediated by an enhanced blockade of intestinal cholesterol absorption. Interestingly, only divalent cations enhanced the cholesterol-lowering effect of plant sterols, thus supporting the idea that the lipid-lowering effect of divalent cations is related to the formation of insoluble and inabsorbable calcium and magnesium chelates with fatty acids. CONCLUSIONS: Our findings indicate that the cholesterol-lowering effect of plant sterols is enhanced by the co-administration of divalent calcium and magnesium cations but not by monovalent sodium and potassium cations.