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Background: Double-strand break repair protein (RAD50) gene plays important roles in genomic integrity, DNA double-strand break repair, cell cycle checkpoint activation, telomere maintenance, and meiotic recombination. The risk allele of RAD50 may negatively affect cancer by reducing the DNA repair capacity. Additionally, Sodium intake and Helicobacter pylori (H. pylori) infection are major risk factors for gastric cancer (GC). Our study investigated the association between polymorphisms in RAD50 gene and the risk of GC case-fatality. We evaluated whether the association differed with sodium intake or H. pylori infection. Methods: We enrolled 490 patients from two hospitals between 2002 and 2006. Their survival or death was prospectively followed up until December 31, 2016, through a review of medical records and telephone surveys. The GC survival was assessed using the Cox proportional hazards regression analysis. Results: In 319 GC cases, the total person-years were 1928.3, and the median survival years was 5.4 years. A total of 137 GC deaths were recorded. Our fully adjusted model showed that the GG type of RAD50 rs17772583 polymorphism is significantly associated with an increased risk of GC case-fatality (hazard ratio [HR] = 2.20, 95% confidence interval [CI] = 1.28–3.77) compared to that associated with the homozygous AA type. In the high sodium intake group, patients with the GG type of RAD50 rs17772583 showed a significantly higher GC case-fatality (HR = 8.61, 95% CI = 2.58–26.68) than that of patients with homozygous AA type. In the positive-H. pylori infection group, patients with GG-type RAD50 rs17772583 showed a significantly higher GC case-fatality (HR = 10.11, 95% CI = 2.81–36.35) than that of with AA homozygotes. Conclusions: Patients with GG-type RAD50 rs17772583, high sodium intake, or a positive-H. pylori infection are at a significantly increased risk of GC case-fatality compared to that associated with the absence of these risk factors. [ABSTRACT FROM AUTHOR]

Purpose: The currently recommended treatment strategy for cystine stone formers is based on a progressive approach that starts with the most conservative measures. In patients with cystinuria, increased patient compliance with dietary management and medical treatment is associated with fewer stone interventions. In this case-based review, the dietary management of cystine stone former was reviewed under the guidance of evidence-based medicine. Methods: The dietary management of the 13-year-old cystinuria patient, who underwent 18 endourological stone interventions, was reviewed in the light of evidence-based medicine. A literature search was performed in Pubmed, MEDLINE, Embase, and Cochrane Library databases according to PRISMA guidelines published from 1993 to September 2022. A total of 304 articles were included in this paper. Results: In managing patients with cystinuria, hyperhydration, and alkalinization of the urine with medical treatment, the rational use of cystine-binding drugs by taking into account individual situations has come to the fore. A limited study has argued that a vegetarian diet is effective as the alkaline load from fruits and vegetables can reduce the amount of alkalizing substances required to achieve urinary alkalinization above pH 7.5, making it particularly suitable for the dietary treatment of cystine stone disease. Conclusion: Life-long follow-up with dietary modification, hyperhydration, and personalized medical therapy (alkalinization and cystine-binding drugs) are critical in preventing chronic kidney disease and kidney failure in cystinuria. [ABSTRACT FROM AUTHOR]

Objectives: High salt intake results in various harmful effects on human health including hypertension, cardiovascular disease, and reduced bone density. Despite this, there are very few studies in the literature that have investigated the association between sodium intake and osteoarthritis (OA). Therefore, we aimed to explore these associations in a Korean population. Methods: This study used cross-sectional data from adult subjects aged 50–75 years from two consecutive periods of the Korean National Health and Nutrition Examination Survey V–VII (2010–2011 and 2014–2016). The estimated 24-hour urinary sodium excretion (24HUNa) was used as a surrogate marker of salt intake. In the 2010–2011 dataset, knee OA (KOA) was defined as the presence of the radiographic features of OA and knee pain. The association between KOA and salt intake was analysed using univariable and multivariable logistic regression methods. For the sensitivity analysis, the same procedures were conducted on subjects with self-reported OA (SR-OA) with knee pain in the 2010–2011 dataset and any site SR-OA in the 2014–2016 dataset. Results: Subjects with KOA had significantly lower energy intake, but higher 24HUNa than those without KOA. The restricted cubic spline plots demonstrated a J-shaped distribution between 24HUNa and prevalent KOA. When 24HUNa was stratified into five groups (<2, 2–3, 3–4, 4–5 and ≥5 g/day), subjects with high sodium intake (≥5 g/day) had a higher risk of KOA (odds ratio [OR] = 1.64, 95% confidence interval [CI] 1.03–2.62) compared to the reference group (3–4 g/day) after adjusting for covariates. The sensitivity analysis based on SR-OA with knee pain showed that high sodium intake was also significantly associated with increased prevalence of OA (OR = 1.84, 95% CI 1.10–3.10) compared with the reference group. Regarding SR-OA at any site in the 2014–2016 dataset, estimated 24HUNa showed a significantly positive association with the presence of SR-OA after adjusting for potential confounders. Conclusions: This nationwide Korean representative study showed a significant association between symptomatic KOA and high sodium intake (≥5 g/day). Avoidance of a diet high in salt might be beneficial as a non-pharmacologic therapy for OA. [ABSTRACT FROM AUTHOR]

Abrupt changes in food preferences and eating habits have induced an overlooked health risk during the coronavirus disease pandemic (COVID-19). Indeed, emerging evidence points to a major shift to consumption of high-sodium foods during the pandemic lockdowns in the population from different countries and cultures. High-sodium foods have sodium contents exceeding 500 mg per 100 g, and many processed and preserved foods fall into this category. Excessive dietary sodium intake is associated with chronic diseases including hypertension, cardiovascular diseases, and kidney diseases, and thus poses confounding risks during the pandemic. Here, we review food categories in consumers' shopping lists and food parcels delivered to people who needed assistance during the pandemic, when frozen meals, canned foods, instant foods, snacks, and other high-sodium foods gained substantial popularity. Such change in consumers' behavior is driven by several factors: the perceived risk of viral infection in grocery shopping trips, limited supplies and inflated prices of fresh produce, preference on foods with long shelf lives, and emotional eating. Moreover, the general low awareness of sodium contents in food has contributed to the increased consumption of high-sodium foods during the pandemic. We also discuss the possible effects on COVID-19 infection and severity caused by excessive sodium intake. We conclude that the public should be educated to maintain a healthy sodium intake during the pandemic, and measures should be adopted by governments and private donors in procuring food parcels with more balanced sodium contents to lower the risks of prolonged and excessive sodium intakes in the vulnerable population. [ABSTRACT FROM AUTHOR]

Purpose of Review: Excessive dietary salt intake is associated with an increased risk of hypertension. Salt sensitivity, i.e., an elevation in blood pressure in response to high dietary salt intake, has been associated with a high risk of cardiovascular disease and mortality. We investigated whether a causal association exists between dietary sodium intake and hypertension risk using Mendelian randomization (MR). Recent Findings: We performed an MR study using data from a large genome-wide association study comprising 15,034 Korean adults in a community-based cohort study. A total of 1282 candidate single nucleotide polymorphisms associated with dietary sodium intake, such as rs2960306, rs4343, and rs1937671, were selected as instrumental variables. The inverse variance weighted method was used to assess the evidence for causality. Higher dietary sodium intake was associated with salt-sensitive hypertension risk. The variants of SLC8E1 rs2241543 and ADD1 rs16843589 were strongly associated with increased blood pressure. In the logistic regression model, after adjusting for age, gender, smoking, drinking, exercise, and body mass index, the GRK4 rs2960306TT genotype was inversely associated with hypertension risk (OR, 0.356; 95% CI, 0.236–0.476). However, the 2350GG genotype (ACE rs4343) exhibited a 2.11-fold increased hypertension risk (OR, 2.114; 95% CI, 2.004–2.224) relative to carriers of the 2350AA genotype, after adjusting for confounders. MR analysis revealed that the odds ratio for hypertension per 1 mg/day increment of dietary sodium intake was 2.24 in participants with the PRKG1 rs12414562 AA genotype. Summary: Our findings suggest that dietary sodium intake may be causally associated with hypertension risk. [ABSTRACT FROM AUTHOR]

Purpose: Subclinical vascular damage is a chronic intermediate process in cardiovascular disease (CVD) and high sodium (Na) has been regarded as an adverse factor in subclinical vascular health; however, the longitudinal relationship between Na intake and subclinical vascular damage has not been studied. We aimed to evaluate the longitudinal relationship of dietary Na intake and sodium to potassium ratio (Na:K) with brachial-ankle pulse wave velocity (baPWV) and carotid intima media thickness (cIMT) in healthy adults aged 40 years and older in Korea. Methods: The present study was based on participants (n = 2145 for baPWV analysis and n = 2494 for cIMT analysis) who visited three times during 2005–2013 (median 5.3 years of follow-up). We used both dietary Na intake and Na:K at baseline and its average (baseline, 2nd, 3rd), which was obtained from food frequency questionnaire (FFQ) as exposure at every visit. baPWV and cIMT levels at the third visit and change from baseline to the third visit were used to represent the level of subclinical vascular damage. Results: After adjustment for potential confounders, significant positive relationships between dietary Na intake and both baPWV3rd and cIMT3rd were observed (baPWV: p for trend ≤ 0.0001 for Naaverage; cIMT: p for trend = 0.013 for Naaverage). Compared with Na:Ks less than 1.0, the levels of both baPWV and cIMT were higher for participants with Na:Ks over 1.0 (baPWV: p for trend = 0.0002 for Na:Kaverage; cIMT: p for trend = 0.005 for Na:Kaverage). Similar significant trends were shown in relationships between dietary Na intake and Na:K and changes in baPWV and cIMT levels. Conclusions: In conclusion, dietary Na intake and Na:K may be positively linked to subsequent baPWV and cIMT levels in adults aged 40 years and older in Korea. Our findings may provide informative evidence on subclinical vascular damage, particularly for populations with relatively high dietary Na intake and low dietary K intake. [ABSTRACT FROM AUTHOR]

Objective: The aim of this study was to determine how sodium intake can affect frailty, but not anorexia, in community-dwelling older adults in Korea. Design: This was a cross-sectional study. Setting: The study used data from the Korean Frailty and Aging Cohort Survey (KFACS), a multi-center longitudinal study addressing 10 centers across urban, rural, and suburban communities in Korea, between 2016 and 2017. Participants: A total of 954 older adults who underwent both 24-hour dietary recall assessment and physical function test during the first-year baseline investigation of the KFACS. Measurements: Frailty was determined according to the Fried frailty index (FFI). Results: Of the 954 participants, 461 (48.3%) were male and the mean age was 76.3 years old. The average daily sodium intake was 3857 mg. The frailty prevalence in first to third quartiles was 21.8%, 7.5%, and 5.4%, respectively, and increased in the fourth quartile of sodium intake to 8.9%. Using the second quartile of sodium intake (2504–3575 mg) as reference, the odds ratios of frailty were 1.64 (95% confidence interval: 0.84–3.22), 1.33 (0.57–3.06), and 4.00 (1.72–9.27) for the first (<2504 mg), third (3575–4873 mg), and fourth (≥4873 mg) quartiles, respectively, in a multivariate-adjusted analysis. Conclusion: Low sodium intake (<2504 mg) is related to frailty in older people, but it seems to be a less important factor than other nutritional factors. The prevalence of frailty did not increase up to a daily sodium intake of 3575 mg, but it increased upon a daily sodium intake higher than 3575 mg. [ABSTRACT FROM AUTHOR]

The increasing prevalence of type 2 diabetes mellitus (T2DM) and its complications including cardiovascular disease and chronic kidney disease threaten Korean Americans (KAs). High dietary sodium intake contributes to both conditions. The purpose of the study was to assess dietary sodium consumption and to examine the predictors of sodium intake among KA with T2DM. A total 232 KA who had uncontrolled diabetes participated in this study. The majority of the sample (69%) consumed more sodium than current national guidelines. A high level of energy intake was the strongest predictor for sodium intake with gender and marital status also related. Our findings identified predictive factors to excessive sodium intake and these data support the need for culturally-tailored education about appropriate dietary sodium and energy intake are needed for patients about T2DM. [ABSTRACT FROM AUTHOR]

Purpose: To estimate total sodium (Na) and potassium (K) intake using non-fasting morning urine specimens among Lebanese elementary (6-10 year old) schoolchildren. Method: A national cross-sectional study was conducted. A multistage cluster sampling procedure was used to select a representative sample of 1403 healthy children from the eight districts of Lebanon. Age, anthropometric measurements, and urine samples were collected and analyzed for Na, K, and creatinine (Cr). Results: The ratios of Na and K to Cr were 23.93 ± 15.54 mM/mM (4.86 ± 3.16 mg/mg) and 11.48 ± 5.82 mM/mM (3.97 ± 2.01 mg/mg), respectively, and showed differences ( P value <0.001) between age groups. No differences were found between boys and girls in all the measured Na and K parameters. The estimated mean Na intake was 96.57 ± 61.67 mM/day (2.220 ± 1.418 g/day or 5.69 ± 3.64 g NaCl/day) and exceeded the upper limit of intake in half the children. Estimated K intake was 46.6 ± 23.02 mM/day (1.822 ± 0.900 g/day), and almost all children failed to meet the recommended daily K intake. The high Na/K ratio (2.361 ± 1.67 mM/mM or 1.39 ± 0.98 mg/mg) resulted from a combination of high Na and low K intake but was mostly affected by K intake. Conclusions: About 50 % of children exceeded the recommended daily upper intake for Na, while the majority was below K adequate intake. This unfavorable Na/K ratio is indicative of potentially negative health effects at later stages in life. Interventions aimed at reducing salt intake and increasing consumption of fruits and vegetables are warranted. [ABSTRACT FROM AUTHOR]

Purpose: It is often reported that Na intake levels are higher in Japan than in western countries. Detailed analysis of food intake and its association with Na intake are necessary for supporting further decreases in Na consumption in Japan. We investigated the association between Na and food intake by food group using data from the Japanese participants of the INTERMAP Study. Method: Results from the Japanese participants of the INTERMAP Study who did not use antihypertensive medication and/or consume a reduced Na diet were used (531 men and 518 women, aged 40-59 years), obtained from four 24-h dietary recalls and two 24-h urine collections from each participant. We developed a classification system with 46 food group classifications; food consumption and Na intake from these groups were compared across quartiles of participants determined by 24-h urinary Na excretion per unit of body weight (UNa/BW). Results: Average daily Na intake from Japanese high-Na foods was 2552 mg/day. Participants with a higher UNa/BW consumed a significantly greater amount of high-Na Japanese foods, such as salted fish ( P = 0.001) and miso soup ( P < 0.001). They also had greater amount of rice ( P = 0.001). Participants with lower UNa/BW consumed a significantly greater amount of western foods, such as bread ( P < 0.001) and milk and dairy products ( P < 0.001). Conclusions: Detailed analyses of various Japanese and western food intakes in addition to Na intake were performed. These results can be used to help draw up effective programs for the reduction in Na intake and prevention of prehypertension/hypertension in the Japanese population. [ABSTRACT FROM AUTHOR]

Summary: The present cross-sectional study performed using data from the Korea National Health and Nutrition Examination Survey in 9526 women older than 18 years of age demonstrates that high sodium intake is associated with lower bone mineral density and sodium intake ≥2000 mg/day is a risk factor for osteoporosis in postmenopausal women. Introduction: Several studies have reported that large amount of dietary sodium intake is highly associated with elevated urinary calcium. However, the direct effect of excessive dietary sodium intake on bone mass, as a risk factor for osteoporosis, is still a controversial issue. The aim of the present study was to assess the relationship between high intake of sodium and lower bone mass and risk of osteoporosis in adult women. Methods: This cross-sectional study was performed using data from the Korea National Health and Nutrition Examination Survey (KNHANES), 2008-2011. Participants ( n = 9526 women older than 18 years) were divided into a premenopausal ( n = 4793) and postmenopausal ( n = 4733) group. Both groups were subdivided into five groups according to quintiles of energy-adjusted sodium intake. Multiple regression analysis was performed to assess relationships between sodium intake and lower bone mass. Results: Multivariate linear regression analysis showed that high sodium intake was negatively associated with bone mineral content (BMC) and bone mineral density (BMD) in postmenopausal women. After adjusting confounding factors, high sodium intake was negatively associated with BMC and BMD of the lumbar spine in postmenopausal women. Postmenopausal women, whose sodium intake was ≥2000 mg/day (odds ratio 1.284, 95% CI 1.029-1.603, P = 0.027), were at risk of developing osteoporosis after adjustment of confounding variables. Conclusions: The present study suggested that high sodium intake could be a potential risk factor for low bone mass after adjusting for confounding factors in postmenopausal women. [ABSTRACT FROM AUTHOR]

Background: Various studies have shown that sodium intake is related to increased blood pressure. However, the relationship between sodium intake and cognitive function and depression has not previously been studied. Aim: The objective of this study was to investigate the relationship between 24-h sodium excretion with cognitive function, depression and sleep quality in patients newly diagnosed with essential hypertension. Methods: All patients underwent history taking, physical examination, blood pressure measurement, 12-lead ECG evaluation, routine urine analysis, biochemical analysis and 24-h urine collection to measure urinary sodium and protein excretion and creatinine clearance, evaluation of cognitive function, depressive behaviour and sleep quality. Results: In total, 119 patients newly diagnosed with essential hypertension (50 men and 69 women aged 54.2 ± 16.1 years) were enrolled. The 24-h urinary sodium excretion of the patients was 204.0 ± 240.4 mEq/day. The Standardized Mini Mental State Examination (SMMSE), Pittsburgh Sleep Quality Index and Beck Depression Inventory scores of the patients were 26.0 ± 2.7, 5.6 ± 3.1 and 21.6 ± 13.5, respectively. Spearman correlation analysis revealed that 24-h urinary sodium excretion was correlated with age (rho −0.258, p = 0.005), systolic blood pressure (rho 0.219, p = 0.017), diastolic blood pressure (rho 0.195, p = 0.034), creatinine clearance (rho 0.414, p < 0.0001) and SMMSE score (rho −0.257, p = 0.005). Stepwise linear regression of independent factors revealed that gender ( p < 0.0001), creatinine clearance ( p < 0.0001), systolic blood pressure ( p = 0.031) and SMMSE score ( p < 0.0001) were independently related to logarithmically converted 24-h sodium excretion. Conclusion: The current study demonstrated that better cognitive function, but not depressive behaviour and sleep disturbance, is related to decreased sodium intake as evaluated by 24-h urinary sodium excretion. Studies are needed to highlight the mechanisms regarding the relationship between cognitive function and sodium intake. [ABSTRACT FROM AUTHOR]

The renin-angiotensin system is essential for body fluid homeostasis and blood pressure regulation. This review focuses on the homeostatic regulation of the secretion of active renin in the kidney, primarily in humans. Under physiological conditions, renin secretion is determined mainly by sodium intake, but the specific pathways involved and the relations between them are not well defined. In animals, renin secretion is a log-linear function of sodium intake. Close associations exist between sodium intake, total body sodium, extracellular fluid volume, and blood volume. Plasma volume increases by about 1.5 mL/mmol increase in daily sodium intake. Several lines of evidence indicate that central blood volume may vary substantially without measurable changes in arterial blood pressure. At least five intertwining feedback loops of renin regulation are identifiable based on controlled variables (blood volume, arterial blood pressure), efferent pathways to the kidney (nervous, humoral), and pathways operating via the macula densa. Taken together, the available evidence favors the notion that under physiological conditions (1) volume-mediated regulation of renin secretion is the primary regulator, (2) macula densa mediated mechanisms play a substantial role as co-mediator although the controlled variables are not well defined so far, and (3) regulation via arterial blood pressure is the exception rather than the rule. Improved quantitative analyses based on in vivo and in silico models are warranted. [ABSTRACT FROM AUTHOR]

Universal reduction in sodium intake has long been recommended, largely because of its proven ability to lower blood pressure for some. However, multiple randomized trials have also demonstrated that similar reductions in sodium increase plasma renin activity and aldosterone secretion, insulin resistance, sympathetic nerve activity, serum cholesterol and triglyceride levels. Thus, the health consequences of reducing sodium cannot be predicted by its impact on any single physiologic characteristic but will reflect the net of conflicting effects. Some 23 observational studies (>360,000 subjects and >26,000 end points) linking sodium intake to cardiovascular outcomes have yielded conflicting results. In subjects with average sodium intakes of less than 4.5 grams/day, most have found an inverse association of intake with outcome; in subjects with average intakes greater than 4.5 grams/day, most reported direct associations. Finally, in two, a 'J-shaped' relation was detected. In addition, three randomized trials have found that heart failure subjects allocated to 1.8 g of sodium have significantly increased morbidity and mortality compared with those at 2.8 g. At the same time, a randomized study in retired Taiwanese men found that allocation to an average intake of 3.8 g improved survival compared with 5.3 g. Taken together, these data provide strong support for a 'J-shaped' relation of sodium to cardiovascular outcomes. Sodium intakes above and below the range of 2.5 to 6.0 grams/day are associated with increased cardiovascular risk. This robust body of evidence does not support universal reduction of sodium intake. [ABSTRACT FROM AUTHOR]

We try to explain why hypercalciuria is absent at diagnosis in some children with an ATP6V1B1 mutation. A 5-month-old girl presented with distal renal tubular acidosis (dRTA) and sensorineural hearing loss. Direct sequencing of the ATP6V1B1 genes disclosed a new homozygous mutation (452 delT) in exon 13. In particular, an absence of hypercalciuria and a normal level of parathyroid hormones were noted. After alkaline therapy, the signs of nephrocalcinosis improved on ultrasound during follow-up. After a review of the literature regarding patients with ATP6V1B1 gene mutations, a young age seemed to be an important factor for normocalciuria. The probable mechanism of normocalciuria and a dynamic mode of calcium excretion in patients with dRTA is proposed. The determinant factors include the degree of systemic acidosis, urine pH, genetic polymorphisms, age, dietary factors, and volume status. Low sodium intake may be a major determinant of normocalciuria in these patients. It is suggested that hypercalciuria is usually absent at diagnosis of dRTA in young infants. Blood pH, plasma bicarbonate concentration, urinary citrate levels, and growth catch-up may be better indicators of adequate alkali therapy in normocalciuric children. Volume contraction, low salt content in infant formula, and alkaline urine in young infants are likely to account for the increased calcium reabsorption. [ABSTRACT FROM AUTHOR]

Background: Dietary quality may impact heart failure outcomes. However, the current status of the dietary quality of persons with heart failure has not been previously reported.Objective: To describe sodium intake, patient factors associated with sodium intake and overall dietary quality in a national sample of persons with heart failure.Design: Analysis of repeated cross-sectional probability sample surveys using data from National Health and Nutrition Examination Surveys (NHANES) of 1999-2000, 2001-2002, 2003-2004 and 2005-2006.Participants: The study sample consisted of 574 persons with self-reported heart failure (mean age = 70 years; 52% women).Measurements: Diet of each survey participant was assessed using single 24 hour recall. Dietary nutrients of interest included sodium, the mainstay of heart failure dietary recommendations, and additionally potassium, calcium, magnesium, fish oils, saturated fat and fiber. Specific dietary goals were based on established guidelines.Results: Mean sodium intake was 2,719 mg, with 34% consuming less than 2,000 mg per day. Patient factors associated with greater sodium intake included male gender, lower education, lower income and no reported diagnosis of hypertension. Mean potassium intake was 2,367 mg/day, with no differences by type of diuretic used or renal disease status. Adherence rates to established guidelines for other nutrients were 13% for calcium, 10% for magnesium, 2% for fish oils, 13% for saturated fat and 4% for fiber.Conclusions: Dietary quality of persons with self-reported heart failure was poor. Public health approaches and clinical dietary interventions are needed for persons with this increasingly prevalent clinical syndrome. [ABSTRACT FROM AUTHOR]

Background: Sodium restriction is commonly recommended as a measure to lower blood pressure and thus reduce cardiovascular disease (CVD) and all-cause mortality. However, some studies have observed higher mortality associated with lower sodium intake.Objective: To test the hypothesis that lower sodium is associated with subsequent higher cardiovascular disease (CVD) and all cause mortality in the Third National Health and Nutrition Examination Survey (NHANES III).Design: Observational cohort study of mortality subsequent to a baseline survey.Participants: Representative sample (n = 8,699) of non-institutionalized US adults age > or = 30, without history of CVD events, recruited between 1988-1994.Measurements and Main Results: Dietary sodium and calorie intakes estimated from a single baseline 24-h dietary recall. Vital status and cause of death were obtained from the National Death Index through the year 2000. Hazard ratio (HR) for CVD mortality of lowest to highest quartile of sodium, adjusted for calories and other CVD risk factors, in a Cox model, was 1.80 (95% CI 1.05, 3.08, p = 0.03). Non-significant trends of an inverse association of continuous sodium (per 1,000 mg) intake with CVD and all-cause mortality were observed with a 99% CI of 0.73, 1.06 (p = 0.07) and 0.86, 1.04 (p = 0.11), respectively, while trends for a direct association were not observed.Conclusion: Observed associations of lower sodium with higher mortality were modest and mostly not statistically significant. However, these findings also suggest that for the general US adult population, higher sodium is unlikely to be independently associated with higher CVD or all-cause mortality. [ABSTRACT FROM AUTHOR]

The newborn rat kidney is not fully developed until approximately 12 days after birth. Several lines of evidence suggest that angiotensin II (AII) participates in the postnatal development of the kidney. The aim of the present study was to analyze proliferating cell nuclear antigen (PCNA), fibronectin, a-smooth muscle-actin (a-SM-actin), and AII expression in renal cortex during development in rats born to mothers that received a normal (control) or increased (experimental) sodium intake during pregnancy. Ninety Wistar rats aged 1, 7, 15, and 30 days from the control and experimental groups were killed and the kidneys removed for histological and immunohistochemical studies. The results showed higher fibronectin, a-SM-actin, PCNA, and AII expression in the glomerular and tubulointerstitial areas of the renal cortex of 1- and 7-day-old animals, which decreased with renal development. The animals from the experimental group showed at 1 day of age a decrease in a-SM-actin, fibronectin, PCNA, and AII expression compared with controls of the same age (P<0.05). In conclusion, our data show that increased sodium intake during pregnancy induces a reduction of a-SM-actin, fibronectin, and PCNA expression in the renal cortex tubulointerstitium and glomeruli of neonatal rats. These alterations may be related to the decrease of AII expression also observed in the renal cortex from these animals. [ABSTRACT FROM AUTHOR]

Aim/hypothesis. The renin-angiotensin-aldosterone system is important in diabetic nephropathy, with the angiotensin-converting-enzyme DD-genotype being a renal risk factor. The D-allele is associated with higher ACE concentrations, but functional consequences in diabetes mellitus are not known. To analyse these consequences, we assessed renal and systemic responsiveness to angiotensin I infusion, with the response to angiotensin II as reference. Methods. Uncomplicated Type 1 (insulin-dependent) diabetic patients with contrasting genotypes (11 II and 11 DD) were studied, during low (50 mmol/24 h) and liberal (200 mmol/24 h) sodium diet, during a euglycaemic clamp. Angiotensin I was infused at 4 and 8 ng·kg-1·min-1, 1 h each, followed by infusions of angiotensin II after a 2-h wash-out period. Results. During low sodium, DD-homozygotes showed higher blood pressure sensitivity to angiotensin I (DD 21±5% vs II 15±5%, p<0.01). With liberal sodium, no differences in blood pressure were detected, whereas angiotensin I induced a higher response of ERPF (DD 40±5% vs II 35±4%, p<0.05) and RVR (DD 105±20% and II 89±16% p<0.05) in DD-homozygotes. Differences were not explained by altered angiotensin II sensitivity. Multiple-linear regression analysis showed that angiotensin I induced responses of blood pressure and renal haemodynamics are higher in subjects carrying the DD-genotype. The magnitude of the responses was modulated by sodium intake and long-term glycaemic control. Conclusion/interpretation. This study showed that responses of blood pressure and renal haemodynamics to angiotensin I are increased in diabetic subjects carrying the DD-genotype. Genotype-associated differences in ACE concentrations could, under certain circumstances, have functional consequenses in uncomplicated Type 1 diabetes mellitus. [ABSTRACT FROM AUTHOR]

Aims/hypothesis. Type I (insulin-dependent) diabetes mellitus is associated with an increased extracellular volume. Sodium restriction might seem a logical form of treatment but data on its renal effects is conflicting. We therefore studied the effects of sodium restriction on renal haemodynamics in uncomplicated Type I diabetes mellitus. Methods. Uncomplicated Type I diabetic patients (n = 24) and matched control subjects (n = 24) were studied twice in random order: after a week of 50 mmol or after 200 mmol sodium intake, respectively. The diabetic patients were studied under normoglycaemic clamp conditions. Glomerular filtration rate and effective renal plasma flow were measured as the clearances of iothalamate and hippuran, respectively. Results. During liberal sodium intake, glomerular filtration, effective renal plasma flow and filtration fraction were similar between the diabetic patients and the control subjects. Sodium restriction decreased the effective renal plasma flow in both groups, whereas glomerular filtration rate only decreased in the control subjects. Consequently, in the diabetic patients, the filtration fraction was increased on low sodium (4.1 ± 8.4 %, p < 0.05 vs liberal sodium). As a consequence, filtration fraction (24.0 ± 2.6 vs 22.1 ± 2.0 %, p < 0.05) and glomerular filtration (119 ± 14 vs 110 ± 13 ml/min, p < 0.05) were higher in the diabetic patients than in the control subjects during sodium restriction. Conclusion/interpretation. Short-term moderate sodium restriction induces relative hyperfiltration in uncomplicated Type I diabetes. This could indicate an increased intraglomerular pressure. Sodium restriction could be an unfavourable preventive approach in diabetes mellitus but its long-term effects are not known. [Diabetologia (2002) 45: ▪–▪] [ABSTRACT FROM AUTHOR]

: Lifestyle factors, such as diet, are believed to be involved in modifying bone health, although the results remain controversial, particularly in children and adolescents. The objective of the study was to identify associations between dietary factors and whole body bone measurements in 10-year-old children. The study was a cross-sectional analysis of a random sample of 105 healthy Danish children, aged 10 years (9.97 ± 0.09). Whole body bone mineral content (BMC) and bone area (BA) were determined by dual-energy X-ray absorptiometry. The influence of diet (7 day food records) on BMC and BA were examined in bi- and multivariate analyses. The mean intakes of calcium, protein, phosphorus and sodium were 1226 mg, 78 g, 1523 mg and 3.3 g, respectively. In bivariate analyses, BMC and BA were strongly positively correlated with height (p<0.001) and weight (p<0.001), and with intakes of energy (p<0.005) and several nutrients. BMC was adjusted for size by including BA, height and weight in the multiple linear regression, and BA was adjusted for size by including height and weight in the multiple linear regression. In multivariate analyses, size-adjusted BMC was positively associated with calcium intake (p = 0.02). Size-adjusted BA was positively associated with dietary protein (p = 0.003), and negatively associated with intakes of sodium (p = 0.048) and phosphorus (p = 0.01). In conclusion, calcium intake was positively associated with bone mineralization. There was a positive association between protein and BA, while for phosphorus and sodium the association was negative. The findings suggest that in addition to calcium, the intake of other nutrients influences bone development in prepubertal children. [ABSTRACT FROM AUTHOR]

Angiotensin II (Ang II) is an important regulator of the function of medullary thick ascending limb of loop of Henle (MTAL). Recent studies showed that changes in Ang II receptor expression occur and underlie changes in the function of proximal tubules during altered sodium intake. The present experiment was designed to determine (1) whether expression of the type 1 Ang II (AT1) receptor in the MTAL is regulated by altered sodium intake, and (2) the specific pathway(s) mediating sodium-induced AT1 expression in the MTAL. Wistar rats were fed a normal sodium (0.5%, NS), low sodium (0.07%, LS), or high sodium (4%, HS) diet for 2 weeks. Northern blot analysis and radioligand binding showed that in rats fed a normal sodium diet the rank of order for both AT1 mRNA expression and receptor density was outer medulla > cortex > inner medulla. Sodium restriction significantly increased both AT1 mRNA expression and receptor density in the outer medulla. In contrast, neither AT1 mRNA expression nor receptor density in the outer medulla was altered by sodium loading. Losartan treatment (3 mg/kg/per day by oral gavage for 2 weeks) prevented low sodium-induced upregulation of the AT1 receptor in the outer medulla, but it had no effect on AT1 expression in the outer medulla of rats fed a normal sodium diet. Highly purified suspensions of MTAL were isolated from rats fed a normal or low sodium diet. Low sodium intake significantly increased AT1 mRNA level by 184% and AT1 receptor density by 58% in MTALs. Primary cultures of MTAL cells were treated with PBS, Ang II (10-8 M), and Ang II + 17 octadecynoic (17 ODYA, 10 μM). Ang II caused about 2-fold increase in AT1 mRNA levels, and this increase was diminished by about 30% by the addition of 17 ODYA. We conclude that (1) sodium restriction but not sodium loading increases AT1 receptor expression in the MTAL, (2) low sodium-induced upregulation of the AT1 receptor in the MTAL is Ang II-dependent, and (3) Ang II-induced upregulation of the AT1 receptor in the MTAL is mediated, at least in part, by cytochrome P450 pathways. [ABSTRACT FROM AUTHOR]

The hemodynamic, hormonal, and renal responses to alterations in dietary potassium were studied in normotensive and hypertensive subjects. In a short-term study, nine normotensive and nine hypertensive young men received a normal diet and low potassium, high potassium, and high potassium/low sodium diets for 1 week, each. The long-term effect of potassium supplementation (normal diet plus 96 mmol KCl/d for 8 weeks) was evaluated in 17 patients with essential hypertension. Blood pressure did not change significantly during short-term alterations of potassium intake but decreased during long-term supplementation (from 152.2±3.5/99.6±1.9 mm Hg to 137.4±2.9/89.1±1.4 mm Hg). High dietary potassium induced a significant but transient natriuresis. Plasma potassium concentration was increased during long- but not during short-term high potassium intake. In contrast to plasma renin activity (PRA) and aldosterone, urinary kallikrein was consistently stimulated during long-term potassium supplementation. The plasma concentrations of adrenaline and noradrenaline were significantly higher in hypertensive than in normotensive subjects and were not markedly altered by the dietary changes. It is concluded that long- but not short-term potassium supplementation lowers blood pressure in patients with essential hypertension. The antihypertensive effect may be mediated by potassium-induced natriuresis, by a stimulation of Na-K-ATPase secondary to increased plasma potassium levels, and/or by a modulation of the renin-angiotensin-aldosterone, kallikrein-kinin, and sympathetic nervous systems. [ABSTRACT FROM AUTHOR]

We have studied the effects of adaptation to low NaCl intakes on hexose transport using suspensions of enterocytes isolated from the jejunum and the rectum of the chicken. Animals (12-13 weeks old) were kept for 11 days on either a high-Na (HS) or a low Na (LS) diet. On day 11, mean serum aldosterone concentration was 46 pg/ml in HS birds and 236 pg/ml in LS birds. Results of transport studies show that: (1) adaptation to a LS diet reduces the cellular 3-oxy-methyl- d-glucose cumulative capacity by 40% in the jejunum and is virtually abolished in the rectum; (2) LS adaptation reduces initial α-methyl- d-glucoside influx (1 mmol/l) by 22% in the jejunum and by 54% in the rectum; (3) the influx of the membrane potential sensor tetraphenyl-phosphonium (TPP) in enterocytes strongly suggests that rectal cells of LS birds are significantly depolarized; (4) the presence of 0.1 mmol/l amiloride increases the capacity of the rectal cells of LS birds to establish a sugar gradient across the membrane; (5) incubation of enterocytes with cytochalasin B increases sugar cumulative capacity of the jejunal cells of both HS and LS birds, and has no effect on the rectal cells of LS birds. We conclude that the effects of LS adaptation on sugar transport may involve a reduction in the membrane electrical potential. [ABSTRACT FROM AUTHOR]

Conscious dogs were used to study whether changes in total renal hemodynamics are responsible for diuresis and natriuresis during an experimental increase in left atrial pressure (LAP). To ensure a controlled dietary sodium intake, the dogs ( n=8) were chronically kept on a high or a low sodium intake diet ( HSI; LSI). After the dogs had completely recovered from surgery (carotid loop, thoracotomy, flank incision), LAP was increased by about 10 cm HO for 60 min by tightening a purse string around the mitral annulus (51 expts). Mean urine volume (V) increased in both groups to a comparable degree. Mean sodium excretion increased somewhat more in HSI dogs, but remained elevated in LSI dogs after the LAP increase. Renal blood flow (electromagnetic flow transducer) and inulin clearance did not change. Renal vascular resistance (RVR) increased by about 20% (HSI) and 15% (LSI). - When the induced LAP increase was terminated, V decreased. RVR decreased in HSI dogs by about −11% and in LSI dogs by about −6% below control values.-It is concluded that volume regulatory mechanisms induced by an experimental LAP increase operate independently of changes in total renal blood flow. [ABSTRACT FROM AUTHOR]

The plasma levels of four osmoregulatory hormones and their target ion-transport systems in the lower intestines of the domestic fowl were determined in order to elucidate their interrelationship and their setpoints in relation to NaCl intake. White Plymouth Rock hens were adapted to six intake levels of NaCl (0.20±0.02-24.7±1.9 mmoles Na·kg bw·day) for 6 weeks. The Na absorption and the Cl secretion of colon and coprodeum were characterized in vitro by the effects of hexoses, amino acids, amiloride, and theophylline on the short-circuit current (SCC) and electrical potential difference (PD). The NaCl-conserving system of the adult chicken is set at low intake levels of NaCl as the 80% range (quantitized by non-linear, logistic regression analyses) of the change in the plasma [ALDO], the amiloride-inhibitable Na absorption of coprodeum and colon (Δ SCC), occurred from 0.18 to 2.3, from 0.9 to 4.3, and from 1.2 to 7.3 mmoles Na·kg bw·day, respectively. These results demonstrate that the amiloride-inhibitable Na absorption of coprodcum is more closely linked to plasma [ALDO] than that of colon. The aminoacid-Na coabsorption of colon increased over exactly the same range of Na intake as the colonic amiloride-inhibitable Na absorption decreased, whereas the hexose-Na coabsorption increased at higher levels of Na intake, from 2 to 11 mmoles Na·kg bw·day. Both these Na absorption types had reached their maximums at 24.7 mmoles Na·kg bw·day, whereas the plasma [AVT] and plasma [PRL], although significantly increased, apparently had not; their 80% range of change occurred from 9.9 to 99 mmoles Na·kg bw·day, and the main changes in plasma osmolity were predicted to occur from 5.4 to 107 mmoles Na·kg bw·day. These results suggest that these colonic and hormonal variables conserve osmotically-free water and operate at high NaCl intake. The theophylline-induced colonic Cl secretion did not change with NaCl intake, whereas the stimulation of SCC in coprodeum decreased with increasing NaCl intake: The main change occurred between 0 and 3.2 mmoles Na·kg bw·day. Thus, all ion-transport capacity disappears in coprodeum with increased dietary NaCl intake, whereas colon maintains its ion-transport capacity (although the nature of the Na transport changes). It is suggested that hormones defending the extracellular volume and composition are regulated close to zero input and output of both NaCl and water, regardless of whether they are NaCl conserving or free-water conserving. Therefore, changes in their stable plasma concentrations occur at the extremes of tolerable range of NaCl intake. [ABSTRACT FROM AUTHOR]

Purpose of Review: To highlight dietary changes shown to be associated with a lower risk of cardiovascular events in epidemiological studies and that have been proven to be effective in preventing cardiovascular diseases in clinical trials Recent Findings: Since dietary changes always involve multiple variables, recent observational and intervention studies on dietary prevention of cardiovascular disease focus not only to the limitation of a single nutrient/food intake but also to the other dietary changes implemented to replace it. Summary: The available evidence supports three major dietary strategies for cardiovascular disease prevention: (1) the replacement of saturated fat with unsaturated fat and/or fiber-rich carbohydrate foods; (2) the reduction of salt intake; (3) the implementation of dietary patterns resembling the traditional Mediterranean diet. This support derives not only from RCTs but also from the combination of large observational cohort studies and relatively short-term randomized trials on cardiovascular risk factors. [ABSTRACT FROM AUTHOR]

Angiotensin I was infused into 16 healthy volunteers, 8 blacks and 8 whites with diastolic blood pressures below 75 mm Hg and the infusion rate increased at 3 min intervals until a diastolic blood pressure of equal to or greater than 95 mm Hg was achieved. Blacks exhibited a significantly greater angiotensin I sensitivity needing 1.8 μg/min as opposed to 3.9 μg/min in whites to achieve the target blood pressure. Plasma renin activities were similar in the two groups, but blacks had significantly higher urinary sodium values than whites, 223 mmol per 24 h as compared to 121 mmol per 24 h. It is concluded that the differences in response could be largely due to differences in dietary sodium intake. These factors need to be carefully considered when using angiotensin I infusion as a pharmacodynamic model for studying the effects of ACE inhibitors. [ABSTRACT FROM AUTHOR]