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Obesity, Sodium Homeostasis, and Arterial Hypertension in Children and Adolescents.
Wójcik, M, Kozioł-Kozakowska, A
Nutrients. 2021;(11)
Abstract
BACKGROUND The relationship between obesity, arterial hypertension, and excessive salt intake has been known for a long time; however, the mechanism of this relationship remains not clear. METHODS The paper presents a current literature review on the relationship between salt consumption and the development of arterial hypertension in children and adolescents with obesity. RESULTS In addition to the traditional theory of hypertension development due to the increase in intravascular volume and disturbances of sodium excretion, recent studies indicate the existence of a complex mechanism related to excessive, pathological secretory activity of adipocytes, insulin resistance, and impaired function of the renin-angiotensin-aldosterone axis. That makes obese children and adolescents particularly vulnerable to the development of salt-sensitive arterial hypertension. Studies performed in many countries have shown that children and adolescents consume more sodium than recommended. It is worth noting, however, that the basis for these recommendations was the extrapolation of data from studies conducted on adults. Moreover, more important than sodium intake is the Na/K ratio and water consumption. CONCLUSION Regardless of the population-wide recommendations on reducing salt intake in children, specific recommendations for overweight and obese patients should be developed.
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2.
Sodium Abnormalities in Cardiac Surgery With Cardiopulmonary Bypass in Adults: A Narrative Review.
Leong, XF, Cheng, M, Jong, B, Hwang, NC, Roscoe, A
Journal of cardiothoracic and vascular anesthesia. 2021;(11):3374-3384
Abstract
Perioperative sodium abnormalities or dysnatremia is not uncommon in patients presenting for cardiac surgery and is associated with increased morbidity and mortality. Both the disease process of heart failure and its treatment may contribute to abnormalities in serum sodium concentration. Serum sodium is the main determinant of serum osmolality, which in turn affects cell volume. Brain cells are particularly vulnerable to changes in serum osmolality because of the nondistensible cranium. The potentially catastrophic neurologic sequelae of rapidly correcting chronic dysnatremia and the time-sensitive nature of cardiac surgery can make the management of these patients challenging. The use of cardiopulmonary bypass to facilitate surgery adds another layer of complexity in the intraoperative management of sodium and water balance. This narrative review examines the definition and classification of dysnatremia. It also covers the etiology and pathophysiology of dysnatremia, implications during cardiac surgery requiring cardiopulmonary bypass, and the perioperative management of dysnatremia.
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3.
Plant HKT Channels: An Updated View on Structure, Function and Gene Regulation.
Riedelsberger, J, Miller, JK, Valdebenito-Maturana, B, Piñeros, MA, González, W, Dreyer, I
International journal of molecular sciences. 2021;(4)
Abstract
HKT channels are a plant protein family involved in sodium (Na+) and potassium (K+) uptake and Na+-K+ homeostasis. Some HKTs underlie salt tolerance responses in plants, while others provide a mechanism to cope with short-term K+ shortage by allowing increased Na+ uptake under K+ starvation conditions. HKT channels present a functionally versatile family divided into two classes, mainly based on a sequence polymorphism found in the sequences underlying the selectivity filter of the first pore loop. Physiologically, most class I members function as sodium uniporters, and class II members as Na+/K+ symporters. Nevertheless, even within these two classes, there is a high functional diversity that, to date, cannot be explained at the molecular level. The high complexity is also reflected at the regulatory level. HKT expression is modulated at the level of transcription, translation, and functionality of the protein. Here, we summarize and discuss the structure and conservation of the HKT channel family from algae to angiosperms. We also outline the latest findings on gene expression and the regulation of HKT channels.
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4.
Recent progress in understanding salinity tolerance in plants: Story of Na+/K+ balance and beyond.
Hussain, S, Hussain, S, Ali, B, Ren, X, Chen, X, Li, Q, Saqib, M, Ahmad, N
Plant physiology and biochemistry : PPB. 2021;:239-256
Abstract
High salt concentrations in the growing medium can severely affect the growth and development of plants. It is imperative to understand the different components of salt-tolerant network in plants in order to produce the salt-tolerant cultivars. High-affinity potassium transporter- and myelocytomatosis proteins have been shown to play a critical role for salinity tolerance through exclusion of sodium (Na+) ions from sensitive shoot tissues in plants. Numerous genes, that limit the uptake of salts from soil and their transport throughout the plant body, adjust the ionic and osmotic balance of cells in roots and shoots. In the present review, we have tried to provide a comprehensive report of major research advances on different mechanisms regulating plant tolerance to salinity stress at proteomics, metabolomics, genomics and transcriptomics levels. Along with the role of ionic homeostasis, a major focus was given on other salinity tolerance mechanisms in plants including osmoregulation and osmo-protection, cell wall remodeling and integrity, and plant antioxidative defense. Major proteins and genes expressed under salt-stressed conditions and their role in enhancing salinity tolerance in plants are discussed as well. Moreover, this manuscript identifies and highlights the key questions on plant salinity tolerance that remain to be discussed in the future.
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5.
The energy cost of the tonoplast futile sodium leak.
Shabala, S, Chen, G, Chen, ZH, Pottosin, I
The New phytologist. 2020;(3):1105-1110
Abstract
Active removal of Na+ from the cytosol into the vacuole plays a critical role in salinity tissue tolerance, but another, often neglected component of this trait is Na+ retention in vacuoles. This retention is based on an efficient control of Na+ -permeable slow- and fast-vacuolar channels that mediate the back-leak of Na+ into cytosol and, if not regulated tightly, could result in a futile cycle. This Tansley insight summarizes our current knowledge of regulation of tonoplast Na+ -permeable channels and discusses the energy cost of vacuolar Na+ sequestration, under different scenarios. We also report on a phylogenetic and bioinformatic analysis of the plant two-pore channel family and the difference in its structure and regulation between halophytes and glycophytes, in the context of salinity tolerance.
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6.
The challenges of diagnosis and management of Gitelman syndrome.
Urwin, S, Willows, J, Sayer, JA
Clinical endocrinology. 2020;(1):3-10
Abstract
Gitelman syndrome is an inherited tubulopathy characterized by renal salt wasting from the distal convoluted tubule. Defects in the sodium chloride cotransporter (encoded by SLC12A3) underlie this autosomal recessive condition. This article focuses on the specific challenges of diagnosing and treating Gitelman syndrome, with use of an illustrative case report. Symptoms relate to decreased serum potassium and magnesium levels, which include muscle weakness, tetany, fatigue and palpitations. Sudden cardiac deaths have been reported. Making a diagnosis may be difficult given its rarity but is important. A knowledge of the serum and urine biochemical picture is vital to distinguish it from a broad differential diagnosis, and application of genetic testing can resolve difficult cases. There is a group of Gitelman syndrome heterozygous carriers that experience symptoms and electrolyte disturbance and these patients should be managed in a similar way, though here genetic investigations become key in securing a difficult diagnosis. Potassium and magnesium replacement is the cornerstone of treatment, though practically this can be hard for patients to manage and often does not fully relieve symptoms even when serum levels are normalized. Challenges arise due to the lack of randomized controlled trials focussing on treatment of this rare disease; hence, clinicians endorse strategies in line with correction of the underlying pathophysiology such as sodium loading or pharmacological treatments, which seem to help some patients. Focussed dietary advice and knowing the best tolerated preparations of potassium and magnesium medications are useful tools for the physician, as well as an awareness of the specific burdens that this patient group face in order to signpost appropriate support.
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7.
An Integrative Review of Cerebral Salt Wasting Syndrome.
Oh, H, Seo, W
The Journal of neuroscience nursing : journal of the American Association of Neuroscience Nurses. 2020;(6):289-294
Abstract
BACKGROUND Although cerebral salt wasting syndrome (CSWS) is widely recognized, its clinical characteristics, diagnostic criteria, and management have not been clearly defined. This study was undertaken to comprehensively review current literature and provide a more complete picture of CSWS. This review also aimed to provide information for nurses on how to differentiate cerebral salt wasting syndrome from syndrome of inappropriate antidiuretic hormone secretion. METHODS An integrative review was performed. Searches were conducted between May and July 2018. The primary information sources were CINAHL, Google Scholar, MEDLINE, PubMed, Scopus, and Web of Science. Included articles were published from 1954 to July 2018. RESULTS The essential features of CSWS are hyponatremia, hypovolemia, and increased urine output. Treatment regimens may be determined based on the acuity and severity of hyponatremia and hypovolemia as well as evident symptoms and signs. CONCLUSION This review may help neuroscience nurses become knowledgeable about CSWS for the drafting of appropriate nursing care plans and also be able to differentiate CSWS from syndrome of inappropriate antidiuretic hormone secretion as early as possible for timely and proper management.
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8.
Evolution and evolving resolution of controversy over existence and prevalence of cerebral/renal salt wasting.
Maesaka, JK, Imbriano, LJ, Miyawaki, N
Current opinion in nephrology and hypertension. 2020;(2):213-220
Abstract
PURPOSE OF REVIEW The topic of hyponatremia is in a state of flux. We review a new approach to diagnosis that is superior to previous methods. It simplifies identifying the causes of hyponatremia, the most important issue being the differentiation of the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) from cerebral/renal salt wasting (RSW). We also report on the high prevalence of RSW without cerebral disease in the general wards of the hospital. RECENT FINDINGS We applied our new approach to hyponatremia by utilizing sound pathophysiologic criteria in 62 hyponatremic patients. Seventeen (27%) had SIADH, 19 (31%) had a reset osmostat, 24 (38%) had RSW with 21 having no evidence of cerebral disease, 1 had Addison's disease, and 1 was because of hydrochlorothiazide. Many had urine sodium concentrations (UNa) less than 30 mmol/l. SUMMARY RSW is much more common than perceived in the general wards of the hospital. It is important to change the terminology from cerebral to RSW and to differentiate SIADH from RSW. These changes will improve clinical outcomes because of divergent therapeutic goals of water-restricting in SIADH and administering salt and water to a dehydrated patient with RSW. The present review will hopefully spur others to reflect and act on the new findings and different approaches to hyponatremia.
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9.
Diagnosis and Management of Disorders of Body Tonicity-Hyponatremia and Hypernatremia: Core Curriculum 2020.
Seay, NW, Lehrich, RW, Greenberg, A
American journal of kidney diseases : the official journal of the National Kidney Foundation. 2020;(2):272-286
Abstract
Overall body fluid concentration is regulated within a narrow range by the concerted action of the hypothalamic-pituitary axis to influence water intake through thirst and water excretion via the effect of vasopressin, or antidiuretic hormone, on renal collecting duct water permeability. Sodium is the principal extracellular cation; abnormalities in overall effective body fluid concentration, or tonicity, manifest as disturbances in serum sodium concentration. Depending on its severity and chronicity, hyponatremia can lead to significant symptoms, primarily related to central nervous system function. Failure to correct hyponatremia can lead to permanent neurologic damage, as can over rapid correction. It is thus essential to stay within specific limits for correction, particularly for chronic hyponatremia. Hypernatremia also leads to central nervous system dysfunction, although goals for its correction rate are less well established. This Core Curriculum article discusses the normal regulation of tonicity and serum sodium concentration and the diagnosis and management of hypo- and hypernatremia.
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10.
Thiazide-Associated Hyponatremia: Clinical Manifestations and Pathophysiology.
Filippone, EJ, Ruzieh, M, Foy, A
American journal of kidney diseases : the official journal of the National Kidney Foundation. 2020;(2):256-264
Abstract
Hyponatremia can complicate thiazide use in a minority of susceptible individuals and can result in significant morbidity and even mortality. Risk factors for thiazide-associated hyponatremia include age, female sex, and possibly low body mass. A genetic susceptibility has recently been uncovered. Although frequently developing early after thiazide treatment initiation, many cases of hyponatremia present after months or years of use. Many cases are asymptomatic or have mild symptoms, but seizures and/or coma may develop, especially in those with acute onset. The pathophysiology is incompletely understood and includes some combination of excessive fluid intake, cation (sodium and potassium) depletion, osmotic inactivation of sodium, and reduced ability to excrete free water. Reduced distal delivery of filtrate, reduced solute load (urea), direct inhibition of the sodium-chloride cotransporter, and increased collecting duct permeability to water mediated by some combination of antidiuretic hormone, prostaglandins, and thiazides themselves may contribute to this diluting defect. The predominant pathophysiologic mechanism(s) varies from patient to patient. The cornerstone of therapy is cessation of thiazide use, cation repletion, and oral fluid restriction. If severely symptomatic, 3% saline solution may be indicated. Overly rapid correction of chronic hyponatremia must be avoided in all cases.