We report on an analysis to explore the association between estimated 24-hour urinary sodium excretion (surrogate for sodium intake) and incident cardiovascular disease (CVD) and mortality. Data were obtained from 398 628 UK Biobank prospective cohort study participants (40-69 years) recruited between 2006 and 2010, with no history of CVD, renal disease, diabetes mellitus or cancer, and cardiovascular events and mortality recorded during follow-up. Hazard ratios between 24-hour sodium excretion were estimated from spot urinary sodium concentrations across incident CVD and its components and all-cause and cause-specific mortality. In restricted cubic splines analyses, there was little evidence for an association between estimated 24-hour sodium excretion and CVD, coronary heart disease, or stroke; hazard ratios for CVD (95% CIs) for the 15th and 85th percentiles (2.5 and 4.2 g/day, respectively) compared with the 50th percentile of estimated sodium excretion (3.2 g/day) were 1.05 (1.01-1.10) and 0.96 (0.92-1.00), respectively. An inverse association was observed with heart failure, but that was no longer apparent in sensitivity analysis. A J-shaped association was observed between estimated sodium excretion and mortality. Our findings do not support a J-shaped association of estimated sodium excretion with CVD, although such an association was apparent for all-cause and cause-specific mortality across a wide range of diseases. Reasons for these differences are unclear; methodological limitations, including the use of estimating equations based on spot urinary data, need to be considered in interpreting our findings.
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http://dx.doi.org/10.1161/HYPERTENSIONAHA.119.14302 | DOI Listing |
Ecotoxicol Environ Saf
January 2025
Institute of Combined Injury, State Key Laboratory of Trauma and Chemical Poisoning, Military Key Laboratory of Nanomedicine, Department of Military Preventive Medicine, Army Medical University, Chongqing 400038, China. Electronic address:
Uranium poisoning, particularly from exposure to Depleted Uranium (DU), occurs when uranyl ions enter the bloodstream and bind primarily to transferrin, osteopontin, and albumin before entering cells via corresponding receptors on renal tubular membranes, leading to cellular damage. Uranium poisoning remains a significant clinical challenge, with no ideal treatment currently available. In this study, we investigate the therapeutic potential of human umbilical cord-derived mesenchymal stem cell exosomes (MSC-EXs) in mice exposed to DU.
View Article and Find Full Text PDFPlant Cell
January 2025
State Key Laboratory of Plant Environmental Resilience, China Agricultural University, Beijing 100193, China.
Salt stress causes ion toxicity in plant cells and limits plant growth and crop productivity. Sodium ions (Na+) are transported out of the cell and sequestered in the vacuole for detoxification under salt stress. The salt excretion system is controlled by the SALT OVERLY SENSITIVE (SOS) pathway, which consists of the calcium sensors SOS3 and SOS3-LIKE CALCIUM BINDING PROTEIN 8, the protein kinase SOS2, and the plasma membrane Na+/H+ antiporter SOS1.
View Article and Find Full Text PDFCardiovasc Endocrinol Metab
March 2025
Department of Food and Nutrition Policy and Planning Research, National Nutrition and Food Technology Research Institute, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Background: Coronary artery disease and hypertension are the leading causes of death and disability worldwide, primarily due to high sodium intake. Therefore, accurate assessment of the status of sodium intake and excretion is crucial. The present study aimed to assess the dietary sodium intake and excretion in Iranian population.
View Article and Find Full Text PDFKidney Med
January 2025
Department of Internal Medicine, Section of Cardiovascular Medicine, Yale University School of Medicine, New Haven, CT.
Rationale & Objective: Peritoneal dialysis (PD) solutions provide both clearance of uremic toxins and sodium and water. An intraperitoneal (IP) solution of icodextrin and glucose designed without the requirement for uremic toxin clearance could provide substantially greater sodium and water removal than PD solutions.
Study Design: We examined varying concentrations of icodextrin and dextrose IP solutions in rats.
Nat Rev Nephrol
January 2025
AHEPA Hospital, School of Medicine, Aristotle University of Thessaloniki, Thessaloniki, Greece.
Diuretic drugs act on electrolyte transporters in the kidney to induce diuresis and are often used in chronic kidney disease (CKD), given that nephron loss creates a deficit in the ability to excrete dietary sodium, which promotes an increase in plasma volume. This rise in plasma volume is exacerbated by CKD-induced systemic and intra-renal activation of the renin-angiotensin-aldosterone-system, which further limits urinary sodium excretion. In the absence of a compensatory decrease in systemic vascular resistance, increases in plasma volume induced by sodium retention can manifest as a rise in systemic arterial blood pressure.
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