Urinary Sodium Excretion and Adherence to the Mediterranean Diet in Older Adults

Despite the well-known benefits of the Mediterranean Diet (MedDiet), data on the sodium intake is scarce. This study aimed to quantify the association between sodium excretion and the adherence to the MedDiet in the elderly. A representative sample of 1500 Portuguese adults (≥65 years) was assessed (1321 were eligible for the present analysis). A 24 h urine sample was collected and analysed for creatinine and sodium. Excessive sodium intake was defined as above 2000 mg/day. The adherence to the MedDiet was assessed by the PREDIMED. A binary logistic regression model was conducted to evaluate the association between urinary sodium excretion and the adherence to the MedDiet. Odds Ratios (OR) and respective 95% Confidence Intervals (95% CI) were calculated. Excessive sodium excretion was observed in 80.0% of men and 91.5% of women whereas a high adherence to the MedDiet was reported by 42.2% of women and 46.4% of men. After adjusting for confounders, excessive sodium excretion was associated with a high adherence to the MedDiet in men (OR = 1.94; 95% CI: 1.03–3.65) but not in women. These results show that the MedDiet can be an important source of sodium and highlight the need for implementing strategies to reduce sodium intake when following a MedDiet.

Urinary sodium excretion is not associated with the incidence of end-stage kidney disease and kidney-related death: results from the UK Biobank

Background: Sodium reduction lowers blood pressure and albuminuria, indicating a hypothesized but yet-to-be proven association between sodium intake and kidney-related endpoints. Objectives: We aimed to investigate the associations of 24-h urinary sodium excretion, reflecting daily sodium intake, with kidney-related outcomes. Methods: Prospective cohort of 444,086 middle- to early late-aged participants from the UK Biobank. The primary outcome was a composite of incident end-stage kidney disease (ESKD) and death due to a kidney-related cause, each of which was separately examined as a secondary outcome. Death due to a non-kidney related cause prior to ESKD was considered a competing event. Results: The mean 24-h urinary sodium excretion estimated from spot urinary biomarkers was 3.3 g. During a median follow-up of 11.8 years, 1,256 composite events occurred. Multivariable-adjusted cause-specific hazards models showed that, with every 1-g increment in 24-h urinary sodium excretion, hazard ratios (95% confidence intervals) were 1.03 (0.91-1.16), 1.08 (0.88-1.32), and 1.01 (0.88-1.16) for the composite outcome, incident ESKD, and kidney-related death, respectively. Similar null results were observed when the exposure was treated as binary (<2 g/d vs. ≥2 g/d) or multicategorical (quartiles). Nonlinear associations were not detected with restricted cubic splines. The findings also held constant in prespecified sensitivity and subgroup analyses. Conclusions: Estimated 24-h urinary sodium excretion was not linearly or nonlinearly associated with the incidence of ESKD or death due to kidney-related causes. Our findings did not support the hypothesized notion that sodium intake should be reduced to prevent kidney-related endpoints at the population level.

Diagnostic Strategies to Identify Patients with Genetic Salt-Losing Tubulopathies

Background: Distinguishing patients with the inherited salt-losing tubulopathies (SLT), Gitelman or Bartter syndrome (GS or BS) from wildtype (WT) patients who purge is difficult. We decided to identify clinical/biochemical characteristics which correctly classify SLT. Methods: 66 patients with possible SLT were recruited to a prospective observational cohort study at the UCL Renal Tubular Clinic (London). 31 datapoints were recorded on each patient. All patients were genotyped for pathogenic mutations in genes which cause SLT; 39 patients had pathogenic variants in genes causing SLT. We obtained similar datasets from cohorts in Taipei and Kobe; the combined dataset comprised 419 patients, 291 had genetically confirmed SLT. London and Taipei datasets were combined to train machine learning (ML) algorithms. These were then tested on the Kobe dataset to determine the best biochemical predictors of genetic confirmation of SLT. Results: Single biochemical variables (e.g. plasma renin) were significantly, but inconsistently different between SLT and WT, in the London and combined cohorts. A decision table algorithm using serum bicarbonate and urinary sodium excretion (FENa) achieved a classification accuracy of 74%. A simpler algorithm based on the FECl achieved a classification accuracy of 61%. This was superior to all of the single biochemical variables identified previously.

Prognostic Value of Biomarkers in Children and Adolescents With Orthostatic Intolerance

Orthostatic intolerance (OI) refers to a series of symptoms that occur during upright standing, which can be relieved when returned to the supine position. OI is a common cause of syncope in children and adolescents. In recent years, more and more studies have been carried out to assess the prognosis of OI by using biomarkers, among which, flow-mediated vasodilation, left ventricular ejection fraction and fractional shortening, hemodynamic change during head-up tilt test, detection of 24-h urinary sodium excretion, body mass index, midregional pro-adrenomedullin, and erythrocytic H2S producing rate are relatively stable, inexpensive, and easy to obtain. With the help of biomarkers, individualized treatment can be carried out to improve the long-term prognosis of children and adolescents with OI. This article reviews the prognostic value of biomarkers in children and adolescents with OI.

Association of Urinary Sodium Excretion and Diabetic Kidney Disease in Patients With Type 2 Diabetes Mellitus: A Cross-Sectional Study

BackgroundDiabetic kidney disease (DKD) is the leading cause of end-stage kidney disease worldwide. Epidemiological evidence of the association between urinary sodium excretion and the presence of DKD in patients with type 2 diabetes mellitus (T2DM) has not yet been well established.MethodsWe performed a cross-sectional study of 1545 patients with T2DM over aged 20 years old from January 2018 to December 2020. Urinary sodium excretion was measured by 24-hour urine samples in inpatients and morning fasting urine samples in outpatients. The associations between urinary sodium excretion and the risks of DKD were examined using stepwise regression analysis, logistic regression analysis and multivariable-adjusted restricted cubic splines (RCS).ResultsRegression analysis showed that urinary sodium was independently associated with urinary albumin to creatinine ratio (UACR) level (P = 0.006) and the risks of DKD (P = 0.042). In multivariable-adjusted RCS analysis, urinary sodium excretion was significantly associated with UACR in all patients (P = 0.008), and exhibited a J-shaped relationship. Logistic regression analysis showed that increased urinary sodium excretion was significantly associated with increased risks of DKD [OR (95% CI); 1.56 (1.07-2.27); P = 0.020]. However, the relationships between urinary sodium excretion and the risks of DKD and albuminuria showed no significance, after further adjustment for HOMA-IR and ba-PWV (brachial-ankle pulse wave velocity) (Both P &gt; 0.05).ConclusionsHigher urinary sodium excretion level was associated with increased risks of DKD among patients with T2DM, dependent of vascular sclerosis and insulin resistance.

Distribution of Cardiac and Renal Corin and Proprotein Convertase Subtilisin/Kexin-6 in the Experimental Model of Cardio-Renal Syndrome of Various Severities

Congestive heart failure (CHF) often leads to progressive cardiac hypertrophy and salt/water retention. However, its pathogenesis remains largely unclarified. Corin, a cardiac serine protease, is responsible for converting proANP and proBNP to biologically active peptides. Although the involvement of corin in cardiac hypertrophy and heart failure was extensively studied, the alterations in corin and proprotein convertase subtilisin/kexin-6 (PCSK6), a key enzyme in the conversion of procorin to corin, has not been studied simultaneously in the cardiac and renal tissues in cardiorenal syndrome. Thus, this study aims to examine the status of PCSK6/corin in the cardiac and renal tissues of rats with CHF induced by the creation of aorto-caval fistula (ACF). We divided rats with ACF into two subgroups based on the pattern of their urinary sodium excretion, namely, compensated and decompensated. Placement of ACF led to cardiac hypertrophy, pulmonary congestion, and renal dysfunction, which were more profound in the decompensated subgroup. Corin immunoreactive peptides were detected in all heart chambers at the myocyte membranal and cytosolic localization and in the renal tissue, especially in the apical membrane of the proximal tubule, mTAL, and the collecting duct. Interestingly, the expression and abundance of corin in both the cardiac ventricles and renal tissues were significantly increased in compensated animals as compared with the decompensated state. Noteworthy, the abundance of PCSK6 in these tissues followed a similar pattern as corin. In contrast, furin expression was upregulated in the cardiac and renal tissues in correlation with CHF severity. We hypothesize that the obtained upregulation of cardiac and renal PCSK6/corin in rats with compensated CHF may represent a compensatory response aiming at maintaining normal Na+ balance, whereas the decline in these two enzymes may contribute to the pathogenesis of avid sodium retention, cardiac hypertrophy, and blunted atrial natriuretic peptide/brain natriuretic peptide actions in decompensated CHF.

Salt-Sensitive Hypertension of the Renal Tubular Cell–Specific NFAT5 (Nuclear Factor of Activated T-Cells 5) Knockout Mice

The kidney plays a crucial role in blood pressure (BP) regulation by controlling sodium reabsorption along the nephron. NFAT5 (nuclear factor of activated T-cells 5) is a transcription factor that is expressed in various tissues including the kidney and is activated at hypertonic conditions as observed in the renal medulla; the role for kidney NFAT5 in BP regulation, however, remains still obscure. In the present study, we generated inducible and renal tubular cell–specific NFAT5 knockout (KO) mice and characterized their phenotype. The NFAT5 KO mice exhibited high BP, hypernatremia, polyuria, and low urinary sodium excretion without significant alterations in the plasma renin activity or aldosterone concentration. The mice fed a high-salt diet further increased BP, revealing salt-sensitive hypertension. The KO mice ehibited the increased gene expression of the epithelial sodium channel. Protein expression of epithelial sodium channel in the membrane fraction was also significantly increased in KO mice than in wild-type mice. Treatment with amiloride, an epithelial sodium channel blocker, corrected high BP, hypernatremia, and decreased urinary sodium excretion in KO mice to the same levels of those in wild-type mice. Finally, the effects of high-salt diet and amiloride in KO mice were confirmed by the radiotelemetry method. In conclusion, these data indicate that renal tubular NFAT5 should play an important role in regulating sodium reabsorption through epithelial sodium channel under high-salt conditions, thereby preventing salt-dependent hypertension.

Intervention to decrease salt intake inadequacy using a control device to monitor and control salt use when cooking at home – iMC SALT preliminary results

Introduction Excessive salt intake is one of the greatest risks to public health, making urgent to propose measures to reduce its intake and bring great benefits to reduce cardiovascular diseases risk. In the Portuguese population, the main source of salt consumption is the salt that is added during food preparation and cooking meals. Purpose The main aim of this study was to assess whether an intervention using a dosing salt device (Salt Control H) in food preparation and cooking has beneficial effects in salt intake. Methods This was a two-arm randomized controlled trial. A total of 88 workers from a public university (50% female; mean age 47.2±11.4 years), were randomly assigned to a intervention (I; n=42) or a control group (C; n=46). The intervention was delivered by health professionals in an occupational medicine setting, asking participants to use a salt control device that delivers the maximum amount of salt to add in food preparation and cooking, according to the number and age of the persons who will consume the meal, during 8 weeks. Primary outcome was the 24-hour urinary sodium excretion (Na24), validated by creatinine coefficient, and secondary outcome was 24-h urinary sodium-to-potassium ratio (Na/K24). Parametric tests were used to assess differences between urinary data stratified by C or I group and Mann-Whitney to evaluate differences between stratified groups according to meet WHO daily recommendations of intake. Results At baseline, there was no significant differences in mean Na24 (C: 3145.5±1420.1 and I:3268.7±1159.8 mg/d, p=0.096) and Na/K24 (C: 2.0±0.9 and I: 2.1±0.8 mg/d, p=0.792) between the two groups. After 8 weeks intervention, a Na24 and Na/K24 non statistically significant decrease was observed in the I group (to 3094.1±1391 and 2.0±0.8 mg/d), as opposed to the C group (to 3262.5±1527.0 and 2.2±0.9 mg/d). The proportion of participants from I group that present Na&lt;2000 mg/d increased (from 17 to 29%) as the proportion of participants that present Na/K24 &lt;1 (from 0 to 12%) without significant differences from C group (p=0.214 for Na &lt;2000 mg/d and p=0.383 for Na/K24 &lt;1). Conclusion The Salt Control H measurement device showed promising results to increase adherence to daily salt intake recommendations. The device is a useful and practical tool for educating individuals about dietary salt doses to add to meals cooked at home. FUNDunding Acknowledgement Type of funding sources: Public grant(s) – National budget only. Main funding source(s): Fundação para a Ciência e Tecnologia Figure 1

Association of Urinary Sodium Excretion and Left Ventricular Hypertrophy in People With Type 2 Diabetes Mellitus: A Cross-Sectional Study

BackgroundIt has been well documented that left ventricular hypertrophy (LVH) is highly associated with the incidence of cardiovascular disease (CVD). Evidence indicated that high sodium intake was closely related with LVH in general population. However, information is not available regarding the association between urinary sodium excretion and LVH in patients with type 2 diabetes mellitus (T2DM). This study aimed to explore the association between urinary sodium excretion and LVH in patients with T2DM.MethodsThis cross-sectional analysis included baseline data from 1,556 individuals with T2DM enrolled in the NanFang Prospective Diabetes Study (NFPDS). Urinary sodium excretion levels were measured from 24-hour urine samples of inpatients and morning fasting urine samples of outpatients. Left ventricular dimensions were assessed by echocardiography. The associations between urinary sodium excretion and the risks of cardiovascular events, LVH and left ventricular mass index (LVMI) were examined using linear regression analysis, logistic regression and restricted cubic splines (RCS).ResultsUrinary sodium excretion levels were positively associated with cardiometabolic risk factors, including systolic blood pressure, body mass index, waist circumference and LVMI (All P&lt;0.001). Odds ratios of the highest quartile of urinary sodium excretion compared with the lowest quartile were 1.80 (95% CI, 1.28-2.54; P=0.001) for LVH and 1.77 (95% CI, 1.06-2.94; P=0.028) for CVD, after adjusted for demographics, lifestyle risk factors and cardiovascular risk factors. Multivariable-adjusted RCS analysis of the association between urinary sodium excretion and LVMI showed a significant association (P=0.001) and lacked evidence of a nonlinear association (P=0.406).ConclusionThis study indicated that high urinary sodium excretion was independently associated with increased risk of LVH and CVD in patients with T2DM, suggesting that control of sodium intake may be valuable for the prevention of diabetic cardiovascular complications.