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1.
Hyperchloremic normal gap metabolic acidosis.
Palmer, BF, Clegg, DJ
Minerva endocrinologica. 2019;(4):363-377
Abstract
Metabolic acidosis is defined as a pathologic process that, when unopposed, increases the concentration of hydrogen ions (H+) in the body and reduces the bicarbonate (HCO3-) concentration. Metabolic acidosis can be of a kidney origin or an extrarenal cause. Assessment of urinary ammonium excretion by calculating the urine anion gap or osmolal gap is a useful method to distinguish between these two causes. Extrarenal processes include increased endogenous acid production and accelerated loss of bicarbonate from the body. Metabolic acidosis of renal origin is due to a primary defect in renal acidification with no increase in extrarenal hydrogen ion production. This situation can occur because either the renal input of new bicarbonate is insufficient to regenerate the bicarbonate lost in buffering endogenous acid as with distal renal tubular acidosis (RTA) or the RTA of renal insufficiency, or the filtered bicarbonate is lost by kidney wasting as in proximal RTA. In either condition, because of loss of either NaHCO3 (proximal RTA) or NaA (distal RTA), effective extracellular volume is reduced and as a result the avidity for chloride reabsorption derived from the diet is increased and results in a hyperchloremic normal gap metabolic acidosis. The RTA of renal insufficiency is also characterized by a normal gap acidosis, however, with severe reductions in the glomerular filtration rate an anion gap metabolic acidosis eventually develops.
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2.
Chloride: from Nutrient to Toxicant.
Geilfus, CM
Plant & cell physiology. 2018;(5):877-886
Abstract
In salinized soils in which chloride (Cl-) is the dominant salt anion, growth of plants that tolerate only low concentrations of salt (glycophytes) is disturbed by Cl- toxicity. Chlorotic discolorations precede necrotic lesions, causing yield reductions. Little is known about the effects of Cl- toxicity on these dysfunctions. A lack of understanding exists regarding (i) the molecular and physiological mechanisms that lead to Cl--induced damage and (ii) the adaptive aspects of induced tolerance to Cl- salinity. Here, mechanistic explanations for the Cl--induced stress responses are proposed and novel ideas and strategies by which glycophytic plants avoid the excessive accumulation of Cl- are reviewed. New experiments are suggested to test the proposed hypotheses. Cl- salinity constrains global food security and thus we urgently need more research into the causes and consequences of Cl- salinity.
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3.
Neuronal chloride and excitability - the big impact of small changes.
Raimondo, JV, Richards, BA, Woodin, MA
Current opinion in neurobiology. 2017;:35-42
Abstract
Synaptic inhibition is a critical regulator of neuronal excitability, and in the mature brain the majority of synaptic inhibition is mediated by Cl--permeable GABAA receptors. Unlike other physiologically relevant ions, Cl- is dynamically regulated, and alterations in the Cl- gradient can have significant impact on neuronal excitability. Due to changes in the neuronal Cl- concentration, GABAergic transmission can bidirectionally regulate the induction of excitatory synaptic plasticity and gate the closing of the critical period for monocular deprivation in visual cortex. GABAergic circuitry can also provide a powerful restraining mechanism for the spread of excitation, however Cl- extrusion mechanisms can become overwhelmed and GABA can paradoxically contribute to pathological excitation such as the propagation of seizure activity.
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4.
Chloride on the Move.
Li, B, Tester, M, Gilliham, M
Trends in plant science. 2017;(3):236-248
Abstract
Chloride (Cl-) is an essential plant nutrient but under saline conditions it can accumulate to toxic levels in leaves; limiting this accumulation improves the salt tolerance of some crops. The rate-limiting step for this process - the transfer of Cl- from root symplast to xylem apoplast, which can antagonize delivery of the macronutrient nitrate (NO3-) to shoots - is regulated by abscisic acid (ABA) and is multigenic. Until recently the molecular mechanisms underpinning this salt-tolerance trait were poorly defined. We discuss here how recent advances highlight the role of newly identified transport proteins, some that directly transfer Cl- into the xylem, and others that act on endomembranes in 'gatekeeper' cell types in the root stele to control root-to-shoot delivery of Cl-.
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5.
Chloride: not simply a 'cheap osmoticum', but a beneficial plant macronutrient.
Wege, S, Gilliham, M, Henderson, SW
Journal of experimental botany. 2017;(12):3057-3069
Abstract
At macronutrient levels, chloride has positive effects on plant growth, which are distinct from its function in photosynthesis..
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6.
[The difference and ratio between serum concentrations of natrium and chlorides in patients with hyponatremia].
Schück, O, Horáčková, M
Vnitrni lekarstvi. 2016;(7-8):629-34
Abstract
UNLABELLED The differential diagnosis of hyponatremia is often difficult. This most frequently occurring disorder of the water and electrolyte metabolism is frequently connected with deviations relating to the acid-base balance (ABB). This survey analyzes the relationship between the changes of the volume of body fluids and ABB and infers to what extent the analysis of combinations of the two disorders can support the differential diagnosis of different forms of hyponatremia (differentiation between the dilution vs. depletion forms). The changes of the total water volume (CTV) and ABB may be presented at the same time in the values of the difference and ratio between serum concentrations of natrium and chlorides (SNa+ - SCl-; SNa+/SCl-). The changes of these quantities are analyzed in the models of pathologies connected through hyponatremia and ABB related deviations: (i) retention of solute-free water (hyponatremia associated with dilution acidosis); (ii) retention Na+ in combination with water retention (hyponatremia associated with dilution and hyperchloremic acidosis); (iii) depletion Na+ combined with water depletion (depletion hyponatremia combined with hypochloremic alkalosis), and (iv) combination of dilution and depletion (hyponatremia which may be associated with different ABB related deviations). This survey specifies the extent to which the applied models are consistent with the existing clinical findings and experience. The examinations SNa+ - SCl- and SNa+/SCl- rely only on routinely used laboratory test methods. Monitoring of these quantities may contribute to continuous assessment of the effect of a chosen therapy. KEY WORDS acid-base balance - depletion hyponatremia - differential diagnosis of hyponatremia - dilution hyponatremia - hyponatremia - retention of solute-free water - body fluid volumes.
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7.
Question 7: For an infant with an equivocal sweat chloride following newborn screening, how likely is a diagnosis of cystic fibrosis?
Groves, T, Robinson, P, Fitzgerald, DA
Paediatric respiratory reviews. 2016;:48-50
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8.
Hyperchloremia - Why and how.
Nagami, GT
Nefrologia : publicacion oficial de la Sociedad Espanola Nefrologia. 2016;(4):347-53
Abstract
Hyperchloremia is a common electrolyte disorder that is associated with a diverse group of clinical conditions. The kidney plays an important role in the regulation of chloride concentration through a variety of transporters that are present along the nephron. Nevertheless, hyperchloremia can occur when water losses exceed sodium and chloride losses, when the capacity to handle excessive chloride is overwhelmed, or when the serum bicarbonate is low with a concomitant rise in chloride as occurs with a normal anion gap metabolic acidosis or respiratory alkalosis. The varied nature of the underlying causes of the hyperchloremia will, to a large extent, determine how to treat this electrolyte disturbance.
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9.
Meta-analysis of high- versus low-chloride content in perioperative and critical care fluid resuscitation.
Krajewski, ML, Raghunathan, K, Paluszkiewicz, SM, Schermer, CR, Shaw, AD
The British journal of surgery. 2015;(1):24-36
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Abstract
BACKGROUND The objective of this systematic review and meta-analysis was to assess the relationship between the chloride content of intravenous resuscitation fluids and patient outcomes in the perioperative or intensive care setting. METHODS Systematic searches were performed of PubMed/MEDLINE, Embase and Cochrane Library (CENTRAL) databases in accordance with PRISMA guidelines. Randomized clinical trials, controlled clinical trials and observational studies were included if they compared outcomes in acutely ill or surgical patients receiving either high-chloride (ion concentration greater than 111 mmol/l up to and including 154 mmol/l) or lower-chloride (concentration 111 mmol/l or less) crystalloids for resuscitation. Endpoints examined were mortality, measures of kidney function, serum chloride, hyperchloraemia/metabolic acidosis, blood transfusion volume, mechanical ventilation time, and length of hospital and intensive care unit stay. Risk ratios (RRs), mean differences (MDs) or standardized mean differences (SMDs) and confidence intervals were calculated using fixed-effect modelling. RESULTS The search identified 21 studies involving 6253 patients. High-chloride fluids did not affect mortality but were associated with a significantly higher risk of acute kidney injury (RR 1.64, 95 per cent c.i. 1.27 to 2.13; P < 0.001) and hyperchloraemia/metabolic acidosis (RR 2.87, 1.95 to 4.21; P < 0.001). High-chloride fluids were also associated with greater serum chloride (MD 3.70 (95 per cent c.i. 3.36 to 4.04) mmol/l; P < 0.001), blood transfusion volume (SMD 0.35, 0.07 to 0.63; P = 0.014) and mechanical ventilation time (SMD 0.15, 0.08 to 0.23; P < 0.001). Sensitivity analyses excluding heavily weighted studies resulted in non-statistically significant effects for acute kidney injury and mechanical ventilation time. CONCLUSION A weak but significant association between higher chloride content fluids and unfavourable outcomes was found, but mortality was unaffected by chloride content.
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10.
Mechanism of chlorite degradation to chloride and dioxygen by the enzyme chlorite dismutase.
Schaffner, I, Hofbauer, S, Krutzler, M, Pirker, KF, Furtmüller, PG, Obinger, C
Archives of biochemistry and biophysics. 2015;:18-26
Abstract
Heme b containing chlorite dismutase (Cld) catalyses the conversion of chlorite to chloride and dioxygen which includes an unusual OO bond formation. This review summarizes our knowledge about the interaction of chlorite with heme enzymes and introduces the biological role, phylogeny and structure of functional chlorite dismutases with differences in overall structure and subunit architecture. The paper sums up the available experimental and computational studies on chlorite degradation by water soluble porphyrin complexes as well as a model based on the active site of Cld. Finally, it reports the available biochemical and biophysical data of Clds from different organisms which allow the presentation of a general reaction mechanism. It includes binding of chlorite to ferric Cld followed by subsequent heterolytic OCl bond cleavage leading to the formation of Compound I and hypochlorite, which finally recombine for production of chloride and O2. The role of the Cld-typical distal arginine in catalysis is discussed together with the pH dependence of the reaction and the role of transiently produced hypochlorite in irreversible inactivation of the enzyme.