High sodium intake is considered an indirect cause of obesity because it is often accompanied by higher energy intake and sugar-sweetened soft drink consumption. High sodium intake is associated with increased inflammatory response in adult patients.

This study shows that high sodium intake is positively associated with adiposity, leptin, and tumor necrosis factor-α independent of total energy intake and sugar-sweetened soft drink consumption in healthy white and African American adolescents. (Read the full article)

US children consume excessive amounts of sodium and substantial amounts of added sugars. Early life exposures to salt and sugar can set taste preferences and health trajectories.

A substantial proportion of toddler meals and other commercial foods meant for children age ≥12 months are of potential concern because of their high sodium content or presence of ≥1 added sugar. (Read the full article)

Title: liothyronine sodium, Cytomel, Triostat
Category: Medications
Created: 12/31/1997 12:00:00 AM
Last Editorial Review: 7/31/2019 12:00:00 AM

Background

Fluid overload in patients undergoing hemodialysis contributes to cardiovascular morbidity and mortality. There is a global trend to lower dialysate sodium with the goal of reducing fluid overload.

Background

Water and solute transport across epithelia can occur via the transcellular or paracellular pathways. Tight junctions play a key role in mediating paracellular ion reabsorption in the kidney. In the renal collecting duct, which is a typical absorptive tight epithelium, coordination between transcellular sodium reabsorption and paracellular permeability may prevent the backflow of reabsorbed sodium to the tubular lumen along a steep electrochemical gradient.

Growing evidence indicates that oxidative and endoplasmic reticular stress, which trigger changes in ion channels and inflammatory pathways that may undermine cellular homeostasis and survival, are critical determinants of injury in the diabetic kidney. Cells are normally able to mitigate these cellular stresses by maintaining high levels of autophagy, an intracellular lysosome-dependent degradative pathway that clears the cytoplasm of dysfunctional organelles. However, the capacity for autophagy in both podocytes and renal tubular cells is markedly impaired in type 2 diabetes, and this deficiency contributes importantly to the intensity of renal injury. The primary drivers of autophagy in states of nutrient and oxygen deprivation—sirtuin-1 (SIRT1), AMP-activated protein kinase (AMPK), and hypoxia-inducible factors (HIF-1α and HIF-2α)—can exert renoprotective effects by promoting autophagic flux and by exerting direct effects on sodium transport and inflammasome activation. Type 2 diabetes is characterized by marked suppression of SIRT1 and AMPK, leading to a diminution in autophagic flux in glomerular podocytes and renal tubules and markedly increasing their susceptibility to renal injury. Importantly, because insulin acts to depress autophagic flux, these derangements in nutrient deprivation signaling are not ameliorated by antihyperglycemic drugs that enhance insulin secretion or signaling. Metformin is an established AMPK agonist that can promote autophagy, but its effects on the course of CKD have been demonstrated only in the experimental setting. In contrast, the effects of sodium-glucose cotransporter–2 (SGLT2) inhibitors may be related primarily to enhanced SIRT1 and HIF-2α signaling; this can explain the effects of SGLT2 inhibitors to promote ketonemia and erythrocytosis and potentially underlies their actions to increase autophagy and mute inflammation in the diabetic kidney. These distinctions may contribute importantly to the consistent benefit of SGLT2 inhibitors to slow the deterioration in glomerular function and reduce the risk of ESKD in large-scale randomized clinical trials of patients with type 2 diabetes.

Background and objectives

This study aimed to investigate the association between in-hospital trajectories of serum sodium and risk of in-hospital and 1-year mortality in patients in hospital.

To the Editor We read the recent article by Klauser et al with great interest. While the potential implications of the findings are exciting, we have several concerns. First, the authors do not explicitly state whether electrocardiogram gating was used in their study. This is an important detail because cardiac motion artifact is a source of artifactual coloration with dual-energy computed tomography (DECT), particularly with dual-source scanners given the approximately 80-millisecond temporal difference between the 2 radiography beams. Furthermore, beam hardening artifact from calcified atheromas and partial volume effect, known sources of artifacts in the 2-material decomposition algorithm of DECT, may largely explain the findings. While patients with gout had higher prevalence of coronary calcification (55 of 59 patients [93%]) and cardiovascular monosodium urate (MSU) deposition (51 of 59 patients [86%]) than controls, the authors do not report whether the 4 patients with gout without coronary calcifications exhibited MSU deposition nor the number of controls or cadaveric hearts with coronary calcification. The images from the article show areas of green pixelization occurring adjacent to calcified plaques on grayscale computed tomography images (eg, Figure 2A and D, left anterior descending artery [yellow arrowhead]), which would favor this artifact hypothesis without additional data.

In Reply We appreciate the valuable comments of Becce et al on our article. We applied prospective electrocardiography gating using a thin-slice cardiac protocol to ensure highest spatial resolution with minimal motion artifact. A noncontrast electrocardiography-gated computed tomography (CT) examination with standardized scan parameters was performed using a 128-slice dual-source CT (SOMATOM Definition Flash; Siemens) with a detector collimation of 2 × 64 × 0.6 mm, rotation time of 0.28 seconds, and prospective electrocardiography triggering for heart rates less than 65 beats per minute (diastolic padding, 70% of RR interval) and more than 65 beats per minute (systolic padding, 40% of RR interval). Axial images were reconstructed with 0.75-mm slice width, increment of 0.5, and a medium-smooth convolution kernel (B26f). When motion artifact was present, it was distinguished by visual analysis of an experienced observer and colorized pixels related to motion were excluded.

Interview with Martin J. O'Donnell, MB, PhD, author of Urinary Sodium and Potassium Excretion and Risk of Cardiovascular Events

Interview with Gervasio A. Lamas, MD, author of Effect of Disodium EDTA Chelation Regimen on Cardiovascular Events in Patients With Previous Myocardial Infarction: The TACT Randomized Trial

Krishnasamy, Karthika, author

Structures of voltage-gated channel with toxins suggest strategies for drug development