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Aldosterone, Inflammation, Immune System, and Hypertension.
Ferreira, NS, Tostes, RC, Paradis, P, Schiffrin, EL
American journal of hypertension. 2021;(1):15-27
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Abstract
Aldosterone is a mineralocorticoid hormone that controls body fluid and electrolyte balance. Excess aldosterone is associated with cardiovascular and metabolic diseases. Inflammation plays a critical role on vascular damage promoted by aldosterone and aggravates vascular abnormalities, including endothelial dysfunction, vascular remodeling, fibrosis and oxidative stress, and other manifestations of end-organ damage that are associated with hypertension, other forms of cardiovascular disease, and diabetes mellitus and the metabolic syndrome. Over the past few years, many studies have consistently shown that aldosterone activates cells of the innate and adaptive immune systems. Macrophages and T cells accumulate in the kidneys, heart, and vasculature in response to aldosterone, and infiltration of immune cells contributes to end-organ damage in cardiovascular and metabolic diseases. Aldosterone activates various subsets of innate immune cells such as dendritic cells and monocytes/macrophages, as well as adaptive immune cells such as T lymphocytes, and, by activation of mineralocorticoid receptors stimulates proinflammatory transcription factors and the production of adhesion molecules and inflammatory cytokines and chemokines. This review will briefly highlight some of the studies on the involvement of aldosterone in activation of innate and adaptive immune cells and its impact on the cardiovascular system. Since aldosterone plays a key role in many cardiovascular and metabolic diseases, these data will open up promising perspectives for the identification of novel biomarkers and therapeutic targets for prevention and treatment of diseases associated with increased levels of aldosterone, such as arterial hypertension, obesity, the metabolic syndrome, and heart failure.
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Molecular Basis, Diagnostic Challenges and Therapeutic Approaches of Bartter and Gitelman Syndromes: A Primer for Clinicians.
Nuñez-Gonzalez, L, Carrera, N, Garcia-Gonzalez, MA
International journal of molecular sciences. 2021;(21)
Abstract
Gitelman and Bartter syndromes are rare inherited diseases that belong to the category of renal tubulopathies. The genes associated with these pathologies encode electrolyte transport proteins located in the nephron, particularly in the Distal Convoluted Tubule and Ascending Loop of Henle. Therefore, both syndromes are characterized by alterations in the secretion and reabsorption processes that occur in these regions. Patients suffer from deficiencies in the concentration of electrolytes in the blood and urine, which leads to different systemic consequences related to these salt-wasting processes. The main clinical features of both syndromes are hypokalemia, hypochloremia, metabolic alkalosis, hyperreninemia and hyperaldosteronism. Despite having a different molecular etiology, Gitelman and Bartter syndromes share a relevant number of clinical symptoms, and they have similar therapeutic approaches. The main basis of their treatment consists of electrolytes supplements accompanied by dietary changes. Specifically for Bartter syndrome, the use of non-steroidal anti-inflammatory drugs is also strongly supported. This review aims to address the latest diagnostic challenges and therapeutic approaches, as well as relevant recent research on the biology of the proteins involved in disease. Finally, we highlight several objectives to continue advancing in the characterization of both etiologies.
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3.
Sensing of tubular flow and renal electrolyte transport.
Verschuren, EHJ, Castenmiller, C, Peters, DJM, Arjona, FJ, Bindels, RJM, Hoenderop, JGJ
Nature reviews. Nephrology. 2020;(6):337-351
Abstract
The kidney is a remarkable organ that accomplishes the challenge of removing waste from the body and simultaneously regulating electrolyte and water balance. Pro-urine flows through the nephron in a highly dynamic manner and adjustment of the reabsorption rates of water and ions to the variable tubular flow is required for electrolyte homeostasis. Renal epithelial cells sense the tubular flow by mechanosensation. Interest in this phenomenon has increased in the past decade since the acknowledgement of primary cilia as antennae that sense renal tubular flow. However, the significance of tubular flow sensing for electrolyte handling is largely unknown. Signal transduction pathways regulating flow-sensitive physiological responses involve calcium, purinergic and nitric oxide signalling, and are considered to have an important role in renal electrolyte handling. Given that mechanosensation of tubular flow is an integral role of the nephron, defective tubular flow sensing is probably involved in renal disease. Studies investigating tubular flow and electrolyte transport differ in their methodology, subsequently hampering translational validity. This Review provides the basis for understanding electrolyte disorders originating from altered tubular flow sensing as a result of pathological conditions.
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4.
Kidney Physiology in Pregnancy.
Beers, K, Patel, N
Advances in chronic kidney disease. 2020;(6):449-454
Abstract
A woman's body undergoes a myriad of changes throughout the course of a normal gestation. The kidneys play a central role in driving adjustments that guarantee maternal and fetal well-being, including a dramatic increase in glomerular filtration rate, alterations in tubular function, and changes in electrolyte and acid/base handling. Early in gestation, systemic vasodilation, driven by both a change in quantity of and response to various hormones, leads to increased renal blood flow and glomerular filtration rate. Vasodilation also results in activation of the renin-angiotensin-aldosterone axis, which combined with changing tubular handling causes alterations in total body stores of electrolytes and total body water, resulting in a lower serum sodium concentration. In addition, mild proteinuria, glucosuria, and a decrease in serum calcium and magnesium are common. The primary acid/base change seen in pregnancy is a mild respiratory alkalosis due to progesterone effects. This article provides an overview of the current understanding of the healthy response of the kidneys to pregnancy, an understanding of which is key to caring for the pregnant patient, and early identification of alterations that may indicate underlying kidney pathology in pregnancy.
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5.
A Journey through the Early Evidence Linking Hydration to Metabolic Health.
Vanhaecke, T, Perrier, ET, Melander, O
Annals of nutrition & metabolism. 2020;:4-9
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Abstract
The idea that water intake or hydration may play an intrinsic, independent role in modulating metabolic disease risk is relatively recent. Here, we outline the journey from early experimental works to more recent evidence linking water and hydration to metabolic health. It has been known for decades that individuals with existing metabolic dysfunction experience challenges to body water balance and have elevated arginine vasopressin (AVP), a key hormone regulating body fluid homeostasis. Later, intervention studies demonstrated that altering fluid balance in these individuals could worsen their condition, suggesting that hydration played a role in modulating glycemic control. More recently, observational and interventional studies in healthy individuals have implicated the hydration-vasopressin axis in the pathophysiology of metabolic diseases. Individuals with higher AVP (or its surrogate, copeptin) are at higher risk for developing type 2 diabetes and components of the metabolic syndrome, an association that remains even when controlling for known risk factors. Supporting preclinical work also suggests a causal role for AVP in metabolic dysfunction. It is known that individuals who habitually drink less fluids tend to have higher circulating AVP, which may be lowered by increasing water intake. In the short term, water supplementation in habitual low drinkers with high copeptin may reduce fasting glucose or glucagon, generating a proof of concept for the role of water supplementation in reducing incident metabolic disease. A large randomized trial is ongoing to determine whether water supplementation for 1 year in subjects with low water intake can meaningfully reduce fasting glucose, risk of new-onset diabetes, and other cardiometabolic risk factors.
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6.
A physiological approach to fluid and electrolyte management of the preterm infant: Review.
Segar, JL
Journal of neonatal-perinatal medicine. 2020;(1):11-19
Abstract
Despite the fact that hundreds of thousands of preterm infants receive parenteral fluids each year, study of optimal fluid and electrolyte management in this population is limited. Compared to older children and adults, preterm infants have an impaired capacity to regulate water and electrolyte balance. Appropriate fluid and electrolyte management is critical for optimal care of low birth weight or sick infants, as fluid overload and electrolyte abnormalities pose significant morbidity. This review highlights basic physiological principles which need to be applied when prescribing parenteral fluids and builds upon published literature to outline a rational approach to initial fluid and electrolyte management of the preterm infant.
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7.
Hydration Status and Cardiovascular Function.
Watso, JC, Farquhar, WB
Nutrients. 2019;(8)
Abstract
Hypohydration, defined as a state of low body water, increases thirst sensations, arginine vasopressin release, and elicits renin-angiotensin-aldosterone system activation to replenish intra- and extra-cellular fluid stores. Hypohydration impairs mental and physical performance, but new evidence suggests hypohydration may also have deleterious effects on cardiovascular health. This is alarming because cardiovascular disease is the leading cause of death in the United States. Observational studies have linked habitual low water intake with increased future risk for adverse cardiovascular events. While it is currently unclear how chronic reductions in water intake may predispose individuals to greater future risk for adverse cardiovascular events, there is evidence that acute hypohydration impairs vascular function and blood pressure (BP) regulation. Specifically, acute hypohydration may reduce endothelial function, increase sympathetic nervous system activity, and worsen orthostatic tolerance. Therefore, the purpose of this review is to present the currently available evidence linking acute hypohydration with altered vascular function and BP regulation.
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Considerations for ultra-endurance activities: part 2 - hydration.
Hoffman, MD, Stellingwerff, T, Costa, RJS
Research in sports medicine (Print). 2019;(2):182-194
Abstract
It is not unusual for those participating in ultra-endurance (> 4 hr) events to develop varying degrees of either hypohydration or hyperhydration. Yet, it is important for ultra-endurance athletes to avoid the performance limiting and potentially fatal consequences of these conditions. During short periods of exercise (< 1 hr), trivial effects on the relationship between body mass change and hydration status result from body mass loss due to oxidation of endogenous fuel stores, and water supporting the intravascular volume being generated from endogenous fuel oxidation and released with glycogen oxidation. However, these effects have meaningful implications during prolonged exercise. In fact, body mass loses well over 2% may be required during some ultra-endurance activities to avoid hyperhydration. Therefore, the typical hydration guidelines to avoid more than 2% body mass loss do not apply in ultra-endurance activities and can potentially result in hyperhydration. Fortunately, achieving the balance of proper hydration during ultra-endurance activities need not be complicated and has been well demonstrated to generally be achieved by simply drinking to thirst and avoiding excessive sodium supplementation with intention of replacing all sodium losses during the exercise.
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9.
Kidney Influence on Fluid and Electrolyte Balance.
Ellison, D, Farrar, FC
The Nursing clinics of North America. 2018;(4):469-480
Abstract
The frontline nurse is confronted daily with patients that have some type of kidney dysfunction or disease. Some renal issues resolve themselves, some disorders can be reversed, and others are permanent. Major complications from kidney impairment discussed are fluid and electrolyte disequilibrium with common problems in volume overload, hyperkalemia, metabolic acidosis, hyperphosphatemia, and hormonal secretion. Each problem is presented with potential clinical manifestations and management.
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Tissue Edema, Fluid Balance, and Patient Outcomes in Severe Sepsis: An Organ Systems Review.
Jaffee, W, Hodgins, S, McGee, WT
Journal of intensive care medicine. 2018;(9):502-509
Abstract
Severe sepsis and septic shock remain among the deadliest diseases managed in the intensive care unit. Fluid resuscitation has been a mainstay of early treatment, but the deleterious effects of excessive fluid administration leading to tissue edema are becoming clearer. A positive fluid balance at 72 hours is associated with significantly increased mortality, yet ongoing fluid administration beyond a durable increase in cardiac output is common. We review the pathophysiologic and clinical data showing the negative effects of edema on pulmonary, renal, central nervous, hepatic, and cardiovascular systems. We discuss data showing increased morbidity and mortality following nonjudicious fluid administration and challenge the assumption that patients who are fluid responsive are also likely to benefit from that fluid. The distinctions between fluid requirement, responsiveness, and tolerance are central to newer concepts of resuscitation. We summarize data in each organ system showing a predictable increase in morbidity and mortality with nonbeneficial fluid administration, providing a better framework for precision in volume management of the patient with severe sepsis.