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The Na/K ratio is considered to be a useful index, the monitoring of which allows an effective Na reduction and K increase, because practical methods (self-monitoring devices and reliable individual estimates from spot urine) are available for assessing these levels in individuals. An intervention trial for lowering the Na/K ratio has demonstrated that a reduction of the Na/K ratio mainly involved Na reduction, with only a small change in K. The present study aimed to clarify the relationship between dietary Na intake and the urinary Na/K molar ratio, using standardized low- and high-salt diets, with an equal dietary K intake, to determine the corresponding Na/K ratio. Fourteen healthy young adult volunteers ingested low-salt (3 g salt per day) and high-salt (20 g salt per day) meals for seven days each. Using a portable urinary Na/K meter, participants measured their spot urine at each voiding, and 24-h urine was collected on the last day of each diet period. On the last day of the unrestricted, low-salt, and high-salt diet periods, the group averages of the 24-h urine Na/K ratio were 4.2, 1.0, and 6.9, while the group averages of the daily mean spot urine Na/K ratio were 4.2, 1.1, and 6.6, respectively. The urinary Na/K ratio tracked changes in dietary salt intake, and reached a plateau approximately three days after each change in diet. Frequent monitoring of the spot urine Na/K ratio may help individuals adhere to an appropriate dietary Na intake.

Salt is composed of Sodium Chloride (NaCl) which in body water becomes essential electrolytes, viz., Sodium (Na + ) and Chloride (Cl - ) ions, including in the blood and other extracellular fluids (ECF). Na + ions are necessary cations in muscle contractions and their depletion will effect all the muscles in body including smooth muscle contraction of blood vessels, a fact which is utilized in lowering the blood pressure. Na+ ions also hold water with them in the ECF. Na + homeostasis in body is maintained by thirst (water intake), kidneys (urinary excretion) and skin (sweating). In Na + withdrawal, body tries to maintain homeostasis as far as possible. However, in certain conditions (e.g., during exercise, intake of drugs and in disorders causing Syndrome of Inappropriate Anti Diuretic Hormone Secretion (SIADH), diuretics, diarrhea) coupled with moderate or severe dietary salt restriction (anorexia nervosa), hyponatremia can get precipitated. Hyponatremia is one end point in the spectrum of disorders caused by severe Na + depletion whereas in moderate depletion it can cause hypohydration (or less total body water) and lower urinary volume (U v ). Moreover, salt sensitivity varies in various populations leading to different responses in relation to dietary Na + intake. Diabetes and Hypertension often co-exist but Na + withdrawal in salt sensitive subjects worsens diabetes though hypertension gets better and reverse occurs in salt loading. Therefore, Na + or salt restriction may be non-physiological. In hypertensive subjects other alternatives to Na + withdrawal could be Potassium (K + ) and Calcium (Ca 2+ ) supplementation. Further studies are required to monitor safety/side effects of salt restriction. [PUBLICATION ABSTRACT]

Background. A clear evidence on the benefits of reducing salt in people with chronic kidney disease (CKD) is still lacking. Salt restriction in CKD may allow better control of blood pressure (BP) as shown in a previous systematic review while the effect on proteinuria reduction remains poorly investigated. Methods. We performed a meta-analysis of randomized controlled trials (RCTs) evaluating the effects of low versus high salt intake in adult patients with non-dialysis CKD on change in BP, proteinuria and albuminuria. Results. Eleven RCTs were selected and included information about 738 CKD patients (Stage 1–4); urinary sodium excretion was 104 mEq/day (95%CI, 76–131) and 179 mEq/day (95%CI, 165–193) in low- and high-sodium intake subgroups, respectively, with a mean difference of −80 mEq/day (95%CI from −107 to −53; p <0.001). Overall, mean differences in clinic and ambulatory systolic BP were −4.9 mmHg (95%CI from −6.8 to −3.1, p <0.001) and −5.9 mmHg (95%CI from −9.5 to −2.3, p <0.001), respectively, while clinic and ambulatory diastolic BP were −2.3 mmHg (95%CI from −3.5 to −1.2, p <0.001) and −3.0 mmHg (95%CI from −4.3 to −1.7; p <0.001), respectively. Mean differences in proteinuria and albuminuria were −0.39 g/day (95%CI from −0.55 to −0.22, p <0.001) and −0.05 g/day (95%CI from −0.09 to −0.01, p = 0.013). Conclusion. Moderate salt restriction significantly reduces BP and proteinuria/albuminuria in patients with CKD (Stage 1–4).

Purpose The World Health Organization recommends reduction of salt intake to < 5 g/day and the use of iodized salt to prevent iodine deficiency states. A high prevalence of excess salt consumption and an inadequate iodine intake has been previously shown in an Italian pediatric population. It was appropriate, therefore, to analyse in the same population the relationship occurring between salt consumption and iodine intake. Methods The study population was made of 1270 children and adolescents. Estimates of salt consumption and iodine intake were obtained by measuring 24 h urinary sodium and iodine excretion. Results The iodine intake increased gradually across quartiles of salt consumption independently of sex, age and body weight ( p  < 0.001). Median iodine intake met the European Food Safety Authority adequacy level only in teenagers in the highest quartile of salt consumption (salt intake > 10.2 g/day). We estimated that approximately 65–73% of the total iodine intake was derived from food and 27–35% from iodized salt and that iodized salt made actually only 20% of the total salt intake. Conclusion In this pediatric population, in face of an elevated average salt consumption, the use of iodized salt was still insufficient to ensure an adequate iodine intake, in particular among teenagers. In the perspective of a progressive reduction of total salt intake, the health institutions should continue to support iodoprophylaxis, in the context of the national strategies for salt reduction. In order for these policies to be successful, in addition to educational campaigns, it is needed that the prescriptions contained in the current legislation on iodoprophylaxis are made compelling through specific enforcement measures for all the involved stakeholders.

Tonicity-responsive enhancer binding protein (TonEBP) protects kidney tubular cells against hypertonicity. Calcineurin inhibitors (CNI) are known to suppress TonEBP by hampering nuclear translocation. Moreover, sodium inversely activates TonEBP. We investigated whether CNI-induced nephrotoxicity in transplant recipients could be due to impaired TonEBP activity, and whether sodium restriction exacerbates the intoxication. Immunohistochemical analysis using biopsy specimens from 128 patients revealed that TonEBP was mainly located in the cytoplasm in cases of CNI nephrotoxicity, while it showed nuclear-cytoplasmic staining in cases of rejection or interstitial fibrosis and tubular atrophy. This suggests that TonEBP transactivation is limited in CNI nephrotoxicity. A retrospective observational analysis of 308 kidney transplant recipients at our institute between 1984 and 2018 showed a positive correlation between dietary salt intake and eGFR slope. A low-salt diet is linked to a rapid annual decline in eGFR, with adjusted odds ratios of 2.40 and a 95% confidence interval of 1.18–4.90. These findings suggest that the recommended salt intake for kidney transplant recipients may require reassessment.

Background As the prevalence of hypertension increases in China, it is advised to use salt-restriction spoons (SRS) as a lifestyle modification. This study aimed to examine the associations between estimated salt consumption, SRS usage, and the hypertension status in individuals with poorly controlled hypertension. Methods Data was collected in Huzhou City, Zhejiang Province, in 2021 using convenience sampling. The analysis involved ordinal logistic regression and restricted cubic splines to assess the relevant factors. Results The study found that 73.34% of the 1215 patients had uncontrolled blood pressure (BP). Urinary excretion was assessed through the utilization of the Kawasaki, INTERSALT, and Tanaka formulas. The outcomes of these three methodologies revealed average daily sodium excretion values of 208.70 (65.65), 154.78 (33.91), and 162.61 (40.87) mmol, respectively. The prevalence of utilizing SRS was found to be 37.78% in this study. Despite the acknowledgment among SRS users of the potential hazards associated with excessive salt consumption, there exists a contradictory pattern of attitudes and behaviors concerning salt reduction. Among individuals with different levels of salt intake (quartiles 1–4, Q1 vs Q4), there was a positive association between limiting salt and hypertension status when controlling for other variables (Kawasaki adjusted OR = 0.58, 95% CI = 0.43–0.79; INTERSALT adjusted OR = 0.62, 95% CI = 0.41–0.92; Tanaka adjusted OR = 0.61, 95% CI = 0.45–0.92, p  < 0.05). Our research also revealed that using or used SRS was a protective factor for blood BP control (adjusted OR = 0.79, 95% CI = 0.64–0.99, P  < 0.05). The restricted cubic spline plots illustrated a monotonic upward relationship between estimated 24-h urinary Na and BP (P-overall association < 0.05; P-non-linear association > 0.05). Conclusions The use of dietary SRS could result in decrease in daily salt intake for BP control in patients with poorly controlled hypertension. To reduce the impact of high BP in China, additional studies are required to create interventions that can enhance the results for patients.

Background Salt restriction is a cornerstone in managing ascites in cirrhotic patients; however, its impact on nutritional status, sarcopenia, and mortality remains unclear. Aim To evaluate the effects of a salt-restricted diet (SRD) on ascites control, body composition, sarcopenia development, and patient survival in cirrhotic patients with decompensated liver disease. Methods This prospective study included 102 patients with grade III ascites, categorized into two groups based on dietary adherence: Salt-Restricted Diet (SRD), ( n  = 46) and Salt-Unrestricted Diet (SUD) ( n  = 56). Sodium intake was assessed using the Dietary Sodium Restriction Questionnaire (DSRQ) and spot urine Na/K ratio. Nutritional status, sarcopenia, ascites control, and six-month mortality were evaluated. Results The SRD group showed better ascites control, with fewer paracentesis sessions per month (1.57 ± 0.65 vs. 4.07 ± 1.43, p  < 0.001). Sarcopenia was more prevalent in the SRD group ( p  < 0.001), with lower SMI (4.88 ± 7.13 vs. 16.7 ± 544.8, p  < 0.001) and TR PMM (19.03 ± 3.68 vs. 71.92 ± 191.9, p  < 0.001). Higher nutritional risk was significantly associated with SRD ( p  = 0.001). Mortality was significantly higher in the SRD group (67.4%) compared to the SUD group (35.7%), p  = 0.001. Multivariate analysis identified sarcopenia (OR = 2.684, p  = 0.006) and SRD (OR = 1.65, p  < 0.001) as independent predictors of mortality. Conclusion While effective in ascites control, sodium restriction may compromise nutritional status, heighten sarcopenia risk, and increase mortality, highlighting the need for a more individualized dietary approach.

Dietary salt intake is a long-debated issue. Increased sodium intake is associated with high blood pressure, leading to salt-sensitive hypertension. Excessive salt intake leads to arterial stiffness in susceptible individuals via impaired nitric oxide action and increased endothelin-1 expression, overactivity of the renal sympathetic nervous system and also via aldosterone-independent activation of the mineralocorticoid receptor. Salt restriction in such individuals reduces blood pressure (BP) values. The optimal level of salt restriction that leads to improved cardiovascular outcomes is still under debate. Current BP and dietary guidelines recommend low sodium intake for the general population. However, a specific category of patients does not develop arterial hypertension in response to sodium loading. In addition, recent research demonstrates the deleterious effects of aggressive sodium restriction, even in heart failure patients. This mini review discusses current literature data regarding the advantages and disadvantages of salt restriction and how it impacts the overall health status.

The salt check sheet developed by Tsuchihashi et al. is widely used in general practice to assess salt intake and the associated diets. However, its appropriateness for the general population has not been assessed alongside 24-h urinary salt excretion monitoring. Therefore, in local residents, we analyzed the correlation between check-sheet scores and 24-h urinary salt excretion levels to determine the appropriateness of the check sheet. We asked 176 local residents to complete the salt check sheet and provide urinary samples; the latter were obtained using a proportional sampling method over a 24-h period. One hundred and forty subjects completed the study (men/women: 23/117, mean±s.d. age: 52.7±19.6 years, blood pressure: 122.3±18.0/74.3±11.1 mm Hg), of whom 51 (36.4%) had hypertension. The total salt check-sheet scores were widely distributed (mean±s.d.: 11.1±4.2 points, range: 0-22 points), and the subjects were divided into the following groups on the basis of salt levels: 29.3% were 'low' (0-8 points), 42.8% were 'medium' (9-13 points), 23.6% were 'high' (14-19 points) and 4.3% were 'very high' (>20 points). The mean 24-h urinary salt excretion level was 8.5±3.3 g. The subjects with higher salt-intake levels tended to have increased 24-h urinary salt excretion levels, with significant differences between the three groups ('low' vs. 'medium' vs. 'high to very high' salt levels: 7.6±2.9 g vs. 8.4±2.8 g vs. 9.6±4.2 g, respectively; P=0.03). The total salt check-sheet scores significantly correlated with the 24-h urinary salt excretion levels (r=0.27; P<0.01). Thus, the salt check sheet is applicable for the general population.