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      Hyponatremia and the Brain

      review-article
      1 , 3 , , 2 , 3
      Kidney International Reports
      Elsevier
      brain edema, hyponatremia, osmolarity, serum sodium

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          Abstract

          Hyponatremia is defined by low serum sodium concentration and is the most common electrolyte disorder encountered in clinical practice. Serum sodium is the main determinant of plasma osmolality, which, in turn, affects cell volume. In the presence of low extracellular osmolality, cells will swell if the adaptation mechanisms involved in the cell volume maintenance are inadequate. The most dramatic effects of hyponatremia on the brain are seen when serum sodium concentration decreases in a short period, allowing little or no adaptation. The brain is constrained inside a nonextensible envelope; thus, brain swelling carries a significant morbidity because of the compression of brain parenchyma over the rigid skull. Serum sodium concentration is an important determinant of several biological pathways in the nervous system, and recent studies have suggested that hyponatremia carries a significant risk of neurological impairment even in the absence of brain edema. The brain can also be affected by the treatment of hyponatremia, which, if not undertaken cautiously, could lead to osmotic demyelination syndrome, a rare demyelinating brain disorder that occurs after rapid correction of severe hyponatremia. This review summarizes the pathophysiology of brain complications of hyponatremia and its treatment.

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          Most cited references102

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          Physiology of cell volume regulation in vertebrates.

          The ability to control cell volume is pivotal for cell function. Cell volume perturbation elicits a wide array of signaling events, leading to protective (e.g., cytoskeletal rearrangement) and adaptive (e.g., altered expression of osmolyte transporters and heat shock proteins) measures and, in most cases, activation of volume regulatory osmolyte transport. After acute swelling, cell volume is regulated by the process of regulatory volume decrease (RVD), which involves the activation of KCl cotransport and of channels mediating K(+), Cl(-), and taurine efflux. Conversely, after acute shrinkage, cell volume is regulated by the process of regulatory volume increase (RVI), which is mediated primarily by Na(+)/H(+) exchange, Na(+)-K(+)-2Cl(-) cotransport, and Na(+) channels. Here, we review in detail the current knowledge regarding the molecular identity of these transport pathways and their regulation by, e.g., membrane deformation, ionic strength, Ca(2+), protein kinases and phosphatases, cytoskeletal elements, GTP binding proteins, lipid mediators, and reactive oxygen species, upon changes in cell volume. We also discuss the nature of the upstream elements in volume sensing in vertebrate organisms. Importantly, cell volume impacts on a wide array of physiological processes, including transepithelial transport; cell migration, proliferation, and death; and changes in cell volume function as specific signals regulating these processes. A discussion of this issue concludes the review.
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            Heterogeneity of astrocytic form and function.

            Astrocytes participate in all essential CNS functions, including blood flow regulation, energy metabolism, ion and water homeostasis, immune defence, neurotransmission, and adult neurogenesis. It is thus not surprising that astrocytic morphology and function differ between regions, and that different subclasses of astrocytes exist within the same brain region. Recent lines of work also show that the complexity of protoplasmic astrocytes increases during evolution. Human astrocytes are structurally more complex, larger, and propagate calcium signals significantly faster than rodent astrocytes. In this chapter, we review the diversity of astrocytic form and function, while considering the markedly expanded roles of astrocytes with phylogenetic evolution. We also define major challenges for the future, which include determining how astrocytic functions are locally specified, defining the molecular controls upon astrocytic fate and physiology and establishing how evolutionary changes in astrocytes contribute to higher cognitive functions.
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              Osmotic demyelination syndrome following correction of hyponatremia.

              The treatment of hyponatremia is controversial: some authorities have cautioned that rapid correction causes central pontine myelinolysis, and others warn that severe hyponatremia has a high mortality rate unless it is corrected rapidly. Eight patients treated over a five-year period at our two institutions had a neurologic syndrome with clinical or pathological findings typical of central pontine myelinolysis, which developed after the patients presented with severe hyponatremia. Each patient's condition worsened after relatively rapid correction of hyponatremia (greater than 12 mmol of sodium per liter per day)--a phenomenon that we have called the osmotic demyelination syndrome. Five of the patients were treated at one hospital, and accounted for all the neurologic complications recorded among 60 patients with serum sodium concentrations below 116 mmol per liter; no patient in whom the sodium level was raised by less than 12 mmol per liter per day had any neurologic sequelae. Reviewing published reports on patients with very severe hyponatremia (serum sodium less than 106 mmol per liter) revealed that neurologic sequelae were associated with correction of hyponatremia by more than 12 mmol per liter per day; when correction proceeded more slowly, patients had uneventful recoveries. We suggest that the osmotic demyelination syndrome is a preventable complication of overly rapid correction of chronic hyponatremia.
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                Author and article information

                Contributors
                Journal
                Kidney Int Rep
                Kidney Int Rep
                Kidney International Reports
                Elsevier
                2468-0249
                01 September 2017
                January 2018
                01 September 2017
                : 3
                : 1
                : 24-35
                Affiliations
                [1 ]Nephrology Division, EpiCURA Hospital, Ath Campus, Ath, Belgium
                [2 ]Division of Internal Medicine, Erasme Hospital Brussels, Brussels, Belgium
                [3 ]Research Unit on Hydromineral Metabolism, Faculty of Medicine, Free University of Brussels, Brussels, Belgium
                Author notes
                [] Correspondence: Fabrice Gankam Kengne, Service de Nephrologie, EpiCURA Ath, 3, Rue Maria Thomée, 1070 Bruxelles, Ath, Ath 7800, Belgium.Service de NephrologieEpiCURA Ath, 3, Rue Maria Thomée, 1070 Bruxelles, Ath, Ath 7800Belgium fgankamk@ 123456ulb.ac.be
                Article
                S2468-0249(17)30373-X
                10.1016/j.ekir.2017.08.015
                5762960
                29340311
                99628ebc-193e-40fe-9639-c8e7e1cde214
                © 2017 International Society of Nephrology. Published by Elsevier Inc.

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                : 8 June 2017
                : 23 August 2017
                : 28 August 2017
                Categories
                Review

                brain edema,hyponatremia,osmolarity,serum sodium
                brain edema, hyponatremia, osmolarity, serum sodium

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