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American Family Physician Feb 2019Acute gastroenteritis is defined as a diarrheal disease of rapid onset, with or without nausea, vomiting, fever, or abdominal pain. In the United States, acute... (Review)
Review
Acute gastroenteritis is defined as a diarrheal disease of rapid onset, with or without nausea, vomiting, fever, or abdominal pain. In the United States, acute gastroenteritis accounts for 1.5 million office visits, 200,000 hospitalizations, and 300 deaths in children each year. Evaluation of a child with acute gastroenteritis should include a recent history of fluid intake and output. Significant dehydration is unlikely if parents report no decrease in oral intake or urine output and no vomiting. The physical examination is the best way to evaluate hydration status. The four-item Clinical Dehydration Scale can be used to determine severity of dehydration based on physical examination findings. In children with mild illness, stool microbiological tests are not routinely needed when viral gastroenteritis is the likely diagnosis. Mild gastroenteritis in children can be managed at home. Oral rehydration therapy, such as providing half-strength apple juice followed by the child's preferred liquids, is the mainstay of treatment for mild dehydration and is as effective as intravenous rehydration for preventing hospitalization and return to the emergency department. Oral rehydration solutions are recommended for moderate dehydration. Ondansetron may be prescribed if needed to prevent vomiting and improve tolerance of oral rehydration solutions. Hospitalization and intravenous fluids are recommended for children who do not respond to oral rehydration therapy plus an antiemetic and patients with severe dehydration (i.e., signs of shock or more than 10% dehydration). Handwashing, breastfeeding, and rotavirus vaccination reduce the incidence of acute gastroenteritis in young children.
Topics: Adolescent; Antiemetics; Bicarbonates; Child; Child, Preschool; Dehydration; Fluid Therapy; Gastroenteritis; Glucose; Humans; Infant; Ondansetron; Potassium Chloride; Severity of Illness Index; Sodium Chloride; Vomiting
PubMed: 30702253
DOI: No ID Found -
The New England Journal of Medicine Nov 2017
Review
Topics: Acute Disease; Heart Failure; Humans; Kidney; Sodium Potassium Chloride Symporter Inhibitors
PubMed: 29141174
DOI: 10.1056/NEJMra1703100 -
Nutrients Mar 2024Potassium is a monovalent cation widely present in nature, where it is not in metallic form, but always in combination with other substances, especially chloride [...].
Potassium is a monovalent cation widely present in nature, where it is not in metallic form, but always in combination with other substances, especially chloride [...].
Topics: Humans; Potassium; Chlorides; Potassium Chloride
PubMed: 38542744
DOI: 10.3390/nu16060833 -
Journal of the American Society of... Sep 2022Observational studies suggest that adequate dietary potassium intake (90-120 mmol/day) may be renoprotective, but the effects of increasing dietary potassium and the...
BACKGROUND
Observational studies suggest that adequate dietary potassium intake (90-120 mmol/day) may be renoprotective, but the effects of increasing dietary potassium and the risk of hyperkalemia are unknown.
METHODS
This is a prespecified analysis of the run-in phase of a clinical trial in which 191 patients (age 68±11 years, 74% males, 86% European ancestry, eGFR 31±9 ml/min per 1.73 m, 83% renin-angiotensin system inhibitors, 38% diabetes) were treated with 40 mmol potassium chloride (KCl) per day for 2 weeks.
RESULTS
KCl supplementation significantly increased urinary potassium excretion (72±24 to 107±29 mmol/day), plasma potassium (4.3±0.5 to 4.7±0.6 mmol/L), and plasma aldosterone (281 [198-431] to 351 [241-494] ng/L), but had no significant effect on urinary sodium excretion, plasma renin, BP, eGFR, or albuminuria. Furthermore, KCl supplementation increased plasma chloride (104±3 to 105±4 mmol/L) and reduced plasma bicarbonate (24.5±3.4 to 23.7±3.5 mmol/L) and urine pH (all <0.001), but did not change urinary ammonium excretion. In total, 21 participants (11%) developed hyperkalemia (plasma potassium 5.9±0.4 mmol/L). They were older and had higher baseline plasma potassium.
CONCLUSIONS
In patients with CKD stage G3b-4, increasing dietary potassium intake to recommended levels with potassium chloride supplementation raises plasma potassium by 0.4 mmol/L. This may result in hyperkalemia in older patients or those with higher baseline plasma potassium. Longer-term studies should address whether cardiorenal protection outweighs the risk of hyperkalemia. NCT03253172.
Topics: Male; Humans; Aged; Middle Aged; Female; Potassium Chloride; Hyperkalemia; Potassium, Dietary; Potassium; Renal Insufficiency, Chronic; Dietary Supplements
PubMed: 35609996
DOI: 10.1681/ASN.2022020147 -
The Cochrane Database of Systematic... May 2023Although acute diarrhoea is a self-limiting disease, dehydration may occur in some children. Dehydration is the consequence of an increased loss of water and... (Meta-Analysis)
Meta-Analysis
BACKGROUND
Although acute diarrhoea is a self-limiting disease, dehydration may occur in some children. Dehydration is the consequence of an increased loss of water and electrolytes (sodium, chloride, potassium, and bicarbonate) in liquid stools. When these losses are high and not replaced adequately, severe dehydration appears. Severe dehydration is corrected with intravenous solutions. The most frequently used solution for this purpose is 0.9% saline. Balanced solutions (e.g. Ringer's lactate) are alternatives to 0.9% saline and have been associated with fewer days of hospitalization and better biochemical outcomes. Available guidelines provide conflicting recommendations. It is unclear whether 0.9% saline or balanced intravenous fluids are most effective for rehydrating children with severe dehydration due to diarrhoea.
OBJECTIVES
To evaluate the benefits and harms of balanced solutions for the rapid rehydration of children with severe dehydration due to acute diarrhoea, in terms of time in hospital and mortality compared to 0.9% saline.
SEARCH METHODS
We used standard, extensive Cochrane search methods. The latest search date was 4 May 2022.
SELECTION CRITERIA
We included randomized controlled trials in children with severe dehydration due to acute diarrhoea comparing balanced solutions, such as Ringer's lactate or Plasma-Lyte with 0.9% saline solution, for rapid rehydration.
DATA COLLECTION AND ANALYSIS
We used standard Cochrane methods. Our primary outcomes were 1. time in hospital and 2.
MORTALITY
Our secondary outcomes were 3. need for additional fluids, 4. total amount of fluids received, 5. time to resolution of metabolic acidosis, 6. change in and the final values of biochemical measures (pH, bicarbonate, sodium, chloride, potassium, and creatinine), 7. incidence of acute kidney injury, and 8.
ADVERSE EVENTS
We used GRADE to assess the certainty of the evidence.
MAIN RESULTS
Characteristics of the included studies We included five studies with 465 children. Data for meta-analysis were available from 441 children. Four studies were conducted in low- and middle-income countries and one study in two high-income countries. Four studies evaluated Ringer's lactate, and one study evaluated Plasma-Lyte. Two studies reported the time in hospital, and only one study reported mortality as an outcome. Four studies reported final pH and five studies reported bicarbonate levels. Adverse events reported were hyponatremia and hypokalaemia in two studies each. Risk of bias All studies had at least one domain at high or unclear risk of bias. The risk of bias assessment informed the GRADE assessments. Primary outcomes Compared to 0.9% saline, the balanced solutions likely result in a slight reduction of the time in hospital (mean difference (MD) -0.35 days, 95% confidence interval (CI) -0.60 to -0.10; 2 studies; moderate-certainty evidence). However, the evidence is very uncertain about the effect of the balanced solutions on mortality during hospitalization in severely dehydrated children (risk ratio (RR) 0.33, 95% CI 0.02 to 7.39; 1 study, 22 children; very low-certainty evidence). Secondary outcomes Balanced solutions probably produce a higher increase in blood pH (MD 0.06, 95% CI 0.03 to 0.09; 4 studies, 366 children; low-certainty evidence) and bicarbonate levels (MD 2.44 mEq/L, 95% CI 0.92 to 3.97; 443 children, four studies; low-certainty evidence). Furthermore, balanced solutions likely reduces the risk of hypokalaemia after the intravenous correction (RR 0.54, 95% CI 0.31 to 0.96; 2 studies, 147 children; moderate-certainty evidence). Nonetheless, the evidence suggests that balanced solutions may result in no difference in the need for additional intravenous fluids after the initial correction; in the amount of fluids administered; or in the mean change of sodium, chloride, potassium, and creatinine levels.
AUTHORS' CONCLUSIONS
The evidence is very uncertain about the effect of balanced solutions on mortality during hospitalization in severely dehydrated children. However, balanced solutions likely result in a slight reduction of the time in the hospital compared to 0.9% saline. Also, balanced solutions likely reduce the risk of hypokalaemia after intravenous correction. Furthermore, the evidence suggests that balanced solutions compared to 0.9% saline probably produce no changes in the need for additional intravenous fluids or in other biochemical measures such as sodium, chloride, potassium, and creatinine levels. Last, there may be no difference between balanced solutions and 0.9% saline in the incidence of hyponatraemia.
Topics: Child; Humans; Bicarbonates; Creatinine; Dehydration; Diarrhea; Hypokalemia; Potassium; Potassium Chloride; Ringer's Lactate; Saline Solution; Sodium
PubMed: 37196992
DOI: 10.1002/14651858.CD013640.pub2 -
Cells Oct 2020The SLC12 family of cation-chloride-cotransporters (CCCs) is comprised of potassium chloride cotransporters (KCCs), which mediate Cl extrusion and sodium-potassium... (Review)
Review
The SLC12 family of cation-chloride-cotransporters (CCCs) is comprised of potassium chloride cotransporters (KCCs), which mediate Cl extrusion and sodium-potassium chloride cotransporters (N[K]CCs), which mediate Cl loading. The CCCs play vital roles in cell volume regulation and ion homeostasis. The functions of CCCs influence a variety of physiological processes, many of which overlap with the pathophysiology of cardiovascular disease. Although not all of the cotransporters have been linked to Mendelian genetic disorders, recent studies have provided new insights into their functional role in vascular and renal cells in addition to their contribution to cardiovascular diseases. Particularly, an imbalance in potassium levels promotes the pathogenesis of atherosclerosis and disturbances in sodium homeostasis are one of the causes of hypertension. Recent findings suggest hypothalamic signaling as a key signaling pathway in the pathophysiology of hypertension. In this review, we summarize and discuss the role of CCCs in cardiovascular disease with particular emphasis on knowledge gained in recent years on NKCCs and KCCs.
Topics: Animals; Cardiovascular Diseases; Evolution, Molecular; Humans; Hypothalamus; Models, Biological; Signal Transduction; Sodium-Potassium-Chloride Symporters
PubMed: 33066544
DOI: 10.3390/cells9102293 -
ASN Neuro 2020Elevated extracellular potassium chloride is widely used to achieve membrane depolarization of cultured neurons. This technique has illuminated mechanisms of calcium... (Review)
Review
Elevated extracellular potassium chloride is widely used to achieve membrane depolarization of cultured neurons. This technique has illuminated mechanisms of calcium influx through L-type voltage sensitive calcium channels, activity-regulated signaling, downstream transcriptional events, and many other intracellular responses to depolarization. However, there is enormous variability in these treatments, including durations from seconds to days and concentrations from 3mM to 150 mM KCl. Differential effects of these variable protocols on neuronal activity and transcriptional programs are underexplored. Furthermore, potassium chloride treatments are criticized for being poor representatives of phenomena and are questioned for their effects on cell viability. In this review, we discuss the intracellular consequences of elevated extracellular potassium chloride treatment , the variability of such treatments in the literature, the strengths and limitations of this tool, and relevance of these studies to brain functions and dysfunctions.
Topics: Action Potentials; Animals; Calcium Channels, L-Type; Humans; Membrane Potentials; Neuromuscular Depolarizing Agents; Neurons; Potassium Chloride
PubMed: 33256465
DOI: 10.1177/1759091420974807 -
International Journal of Molecular... Jan 2021Stroke is one of the major culprits responsible for morbidity and mortality worldwide, and the currently available pharmacological strategies to combat this global... (Review)
Review
Stroke is one of the major culprits responsible for morbidity and mortality worldwide, and the currently available pharmacological strategies to combat this global disease are scanty. Cation-chloride cotransporters (CCCs) are expressed in several tissues (including neurons) and extensively contribute to the maintenance of numerous physiological functions including chloride homeostasis. Previous studies have implicated two CCCs, the Na-K-Cl and K-Cl cotransporters (NKCCs and KCCs) in stroke episodes along with their upstream regulators, the with-no-lysine kinase (WNKs) family and STE20/SPS1-related proline/alanine rich kinase (SPAK) or oxidative stress response kinase (OSR1) via a signaling pathway. As the WNK-SPAK/OSR1 pathway reciprocally regulates NKCC and KCC, a growing body of evidence implicates over-activation and altered expression of NKCC1 in stroke pathology whilst stimulation of KCC3 during and even after a stroke event is neuroprotective. Both inhibition of NKCC1 and activation of KCC3 exert neuroprotection through reduction in intracellular chloride levels and thus could be a novel therapeutic strategy. Hence, this review summarizes the current understanding of functional regulations of the CCCs implicated in stroke with particular focus on NKCC1, KCC3, and WNK-SPAK/OSR1 signaling and discusses the current and potential pharmacological treatments for stroke.
Topics: Homeostasis; Humans; Neurons; Phosphorylation; Protein Serine-Threonine Kinases; Signal Transduction; Sodium Potassium Chloride Symporter Inhibitors; Sodium-Potassium-Chloride Symporters; Stroke; Symporters; WNK Lysine-Deficient Protein Kinase 1; K Cl- Cotransporters
PubMed: 33513812
DOI: 10.3390/ijms22031232 -
Kidney360 Nov 2022Elevated abundance of sodium-chloride cotransporter (NCC) and phosphorylated NCC (pNCC) are potential markers of primary aldosteronism (PA), but these effects may be...
BACKGROUND
Elevated abundance of sodium-chloride cotransporter (NCC) and phosphorylated NCC (pNCC) are potential markers of primary aldosteronism (PA), but these effects may be driven by hypokalemia.
METHODS
We measured plasma potassium in patients with PA. If potassium was <4.0 mmol/L, patients were given sufficient oral potassium chloride (KCl) over 24 hours to achieve as close to 4.0 mmol/L as possible. Clinical chemistries were assessed, and urinary extracellular vesicles (uEVs) were examined to investigate effects on NCC.
RESULTS
Among 21 patients with PA who received a median total dose of 6.0 g (2.4-16.8 g) of KCl, increases were observed in plasma potassium (from 3.4 to 4.0 mmol/L; <0.001), aldosterone (from 305 to 558 pmol/L; 0.01), and renin (from 1.2 to 2.5 mIU/L; <0.001), whereas decreases were detected in uEV levels of NCC (median fold change [FC]=0.71 [0.09-1.99]; 0.02), pT60-NCC (FC=0.84 [0.06-1.66]; 0.05), and pT55/60-NCC (FC=0.67 [0.08-2.42]; 0.02). By contrast, in 10 patients with PA who did not receive KCl, there were no apparent changes in plasma potassium, NCC abundance, and phosphorylation status, but increases were observed in plasma aldosterone (from 178 to 418 pmol/L; 0.006) and renin (from 2.0 to 3.0 mU/L; 0.009). Plasma potassium correlated inversely with uEV levels of NCC ( =0.11; 0.01), pT60-NCC ( =0.11; =0.01), and pT55/60-NCC ( =0.11; =0.01).
CONCLUSIONS
Acute oral KCl loading replenished plasma potassium in patients with PA and suppressed NCC abundance and phosphorylation, despite a significant rise in plasma aldosterone. This supports the view that potassium supplementation in humans with PA overrides the aldosterone stimulatory effect on NCC. The increased plasma aldosterone in patients with PA without KCl supplementation may be due to aldosterone response to posture challenge.
Topics: Humans; Sodium Chloride Symporters; Aldosterone; Potassium Chloride; Renin; Phosphorylation; Potassium; Hyperaldosteronism; Dietary Supplements
PubMed: 36514401
DOI: 10.34067/KID.0003632022 -
Journal of the American Chemical Society Aug 2022Chalcogen bonding (ChB) is rapidly rising to prominence in supramolecular chemistry as a powerful sigma (σ)-hole-based noncovalent interaction, especially for...
Chalcogen bonding (ChB) is rapidly rising to prominence in supramolecular chemistry as a powerful sigma (σ)-hole-based noncovalent interaction, especially for applications in the field of molecular recognition. Recent studies have demonstrated ChB donor strength and potency to be remarkably sensitive to local electronic environments, including redox-switchable on/off anion binding and sensing capability. Influencing the unique electronic and geometric environment sensitivity of ChB interactions through simultaneous cobound metal cation recognition, herein, we present the first potassium chloride-selective heteroditopic ion-pair receptor. The direct conjugation of benzo-15-crown-5 ether (B15C5) appendages to Te centers in a bis-tellurotriazole framework facilitates alkali metal halide (MX) ion-pair binding through the formation of a cofacial intramolecular bis-B15C5 M (M = K, Rb, Cs) sandwich complex and bidentate ChB···X formation. Extensive quantitative H NMR ion-pair affinity titration experiments, solid-liquid and liquid-liquid extraction, and U-tube transport studies all demonstrate unprecedented KCl selectivity over all other group 1 metal chlorides. It is demonstrated that the origin of the receptor's ion-pair binding cooperativity and KCl selectivity arises from an electronic polarization of the ChB donors induced by the cobound alkali metal cation. Importantly, the magnitude of this switch on Te-centered electrophilicity, and therefore anion-binding affinity, is shown to correlate with the inherent Lewis acidity of the alkali metal cation. Extensive computational DFT investigations corroborated the experimental alkali metal cation-anion ion-pair binding observations for halides and oxoanions.
Topics: Anions; Cations; Chalcogens; Chlorides; Metals, Alkali; Potassium Chloride
PubMed: 35930460
DOI: 10.1021/jacs.2c05333