Potassium chloride 0.15% (potassium 20mmol/1litre) / Glucose 10% / Sodium chloride 0.45% infusion 1litre bags
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Potassium chloride 0.15% (potassium 20mmol/1litre) / Glucose 10% / Sodium chloride 0.45% infusion 1litre bags
Therapeutically similar medicines
Similarity is based on WHO Anatomical Therapeutic Chemical (ATC) classification and on a factual NHS dm+d therapeutic-grouping code prefix. Source data: NHS dm+d via TRUD (OGL v3.0), WHO ATC/DDD Index.
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NICE clinical guidance(7)
Intravenous fluid therapy in children and young people in hospital (NG29)
Intravenous fluid therapy in adults in hospital (CG174)
Diarrhoea and vomiting caused by gastroenteritis in under 5s: diagnosis and management (CG84)
Neonatal parenteral nutrition (NG154)
Diabetes (type 1 and type 2) in children and young people: diagnosis and management (NG18)
Acute kidney injury: prevention, detection and management (NG148)
i STAT CG4+ and CHEM8+ cartridges for point-of-care testing in the emergency department (MIB38)
Source: National Institute for Health and Care Excellence (NICE). Contains public sector information licensed under the Open Government Licence v3.0.
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Active and completed clinical studies from ClinicalTrials.gov
Source: ClinicalTrials.gov, a database of the U.S. National Library of Medicine (NLM), National Institutes of Health (NIH). Data accessed via ClinicalTrials.gov API v2. Trial information is provided for research purposes and does not constitute medical advice.
Academic studies and reviews for this medicine's active substance
Showing the 50 most relevant studies.
Reviews & meta-analyses: 3 · Randomised trials: 7 · 1946–2026
Showing the 50 most relevant studies, sorted by most relevant.
L. Ceremużyński, A. Budaj, A. Czepiel, et al.
Cardiovascular Drugs and Therapy, 1999
Chan HY, Li D, Yu AS, et al.
2026
Background Current understanding of acute kidney injury (AKI) risk factors remains largely descriptive, offering limited precision into how specific biomarker values or physiologic thresholds influence susceptibility. We aimed to synthesize knowledge from machine learning models trained across multiple health systems to identify generalizable, value-specific risk drivers and biomarker interactions contributing to AKI risk. Methods We analyzed electronic health records (EHRs) from 785,497 adult inpatients between 2010 and 2019 across nine U.S. academic medical centers within PCORnet. Interpretable gradient boosting machine models were independently developed at each health system to quantify predictor-outcome associations. Meta-regression was applied to integrate these site-level results, characterize nonlinear value-risk relationships, and identify bivariate interactions between predictors. Result Meta-analysis revealed consistent, value-specific risk drivers across health systems. An increase in glucose from 100 mg/dL to 140 mg/dL was associated with a 1.46-fold higher risk of AKI. Chloride and anion gap also demonstrated elevated AKI risk with risk increases overlapping portions of their reference ranges, with anion gap showing a 1.14-fold increase across 4–12 mmol/L and chloride a 1.28-fold increase across 96–100 mEq/L. Electrolytes including potassium, calcium, and sodium showed quadratic associations with AKI risk. Bivariate meta-regression identified interactions between key predictors, highlighting pathways that jointly modulate AKI risk. Conclusion This cross-system meta-analysis synthesizes machine learning-derived evidence into clinically interpretable knowledge, revealing how specific biomarker ranges and interactions modulate AKI risk. By moving beyond surface-level associations to quantitative, generalizable physiologic thresholds, these findings provide actionable insights to enhance risk stratification and personalized prevention in hospital care. Highlights Cross-system meta-analysis uncovered generalizable, value-specific AKI risk drivers Glucose, chloride, and anion gap within reference ranges linked to higher AKI risk Key predictor interactions suggest coordinated pathways jointly modulating AKI risk
Abstract licence: CC BY-NC-ND
W. Rogers, P. H. Segall, H. Mcdaniel, et al.
American Journal of Cardiology, 1979
Weintraub L, Fielding CL, Carli IB, et al.
2026
BackgroundAdministration of intravenous fluids prior to competition is common at major equestrian competitions, yet few studies have evaluated the benefits of this practice.Aims/objectiveThe hypothesis was that pre-ride intravenous fluid therapy would be associated with a lower heart rate and improved laboratory hydration parameters during or after the ride.Methods14 client owned horses entered in a 45 km ride in extreme heat and terrain were randomly assigned to receive IV fluids (IVF) or no IV fluids (NIV) the day before the ride. Blood samples and physical examination findings were collected at 6 time points: Home (T0), check in the day before the ride (T1), 2-3 h after catheterization and treatment (T2), 1 h pre-ride (T3), 32 km into the ride (T4), and the end of the ride (T5). Physical examination and laboratory parameters (bicarbonate, sodium, potassium, chloride, calcium, glucose, lactate, BUN, creatinine, PCV and total protein) were evaluated using 2-way ANOVA.ResultsThe total protein concentration at T2 was 0.5 g/dL lower in the IVF group (95 % CI, -1.0 to -0.01 g/dL) compared with the NIV. The BUN concentration at T4 was 4 mg/dL lower in the IVF group (p = 0.02; 95 % CI, -7.3 to -0.9 mg/dL) compared with the NIV. There was no significant difference in heart rates between the IVF and NIV group (36 ± 5 bpm and 39 ± 3 bpm, respectively; p = 0.23).ConclusionsThe use of intravenous fluids prior to riding in extreme conditions may not have clinically significant hydration benefits.
Abstract licence: CC BY-NC-ND
Juett LA, van der Wolf-Ong J, Gyamfi PA, et al.
2026
- Dehydration
- Water
- Glucose
BackgroundPrevious studies indicate that sports drinks may improve rehydration, compared to water, an effect likely achieved by manufacturing sports drinks to contain carbohydrates and sodium. However, there is a growing preference for natural products and a "food first" approach to sports nutrition. Fruit juices naturally contain similar concentrations of carbohydrates to sports drinks, but fruit juices may produce a more stable blood glucose profile. Fruit juices also naturally contain electrolytes, particularly potassium, but their potential as effective rehydration alternatives to sports drinks, which have higher sodium concentrations, is not well understood. This study compared the rehydration efficacy and glucose responses following consumption of a 100% fruit juice (Raw Hydrate®; FRU), a glucose-based sports drink (SPO), and water (WAT) after exercise-induced hypohydration. Importantly, rehydration beverages were matched for water volume, rather than total volume, to ensure that any potential differences in water balance were not due to unequal water volumes between trials, a limitation affecting previous rehydration research.MethodsAfter familiarization, 17 adults (age: 28 ± 8 years; BMI: 23.8 ± 2.9 kg/m2) completed three trials in a randomized cross-over design. The participants cycled in the heat (~35°C) to induce ~2% body mass loss (BML), then rehydrated over a 1 h period in a laboratory (~21°C) with a water volume equivalent to 150% of BML from either FRU, SPO, or WAT. This was followed by an additional 4 h of seated rest (5 h rehydration period), when blood glucose was measured (0, 0.25, 0.5, 0.75, 1, 1.5, and 2 h after beverage consumption), and all urine produced was collected.ResultsDuring the 5 h rehydration period, there was no effect of trial on total urine volume (FRU: 1266 ± 403 mL, SPO: 1338 ± 361 mL, WAT: 1394 ± 360 mL; P = 0.156) or water retention (FRU: 42 ± 12%, SPO: 37 ± 10%, WAT: 35 ± 11%; P = 0.059). The blood glucose area under the curve differed by trial (P P ConclusionRehydration efficacy was similar between all beverages, but each elicited a distinct glycemic response. For sports drink consumers seeking a natural alternative or implementing a "food first" nutritional strategy, switching to a 100% fruit juice will not compromise rehydration effectiveness, but may elicit a lower blood glucose response. Although, it should be noted that an additional three participants were withdrawn from the study because of gastrointestinal issues after consuming the 100% fruit juice. This was likely a product of the present study's design, where a large volume of 100% fruit juice (average ~2,300 mL) was consumed in a short period of time (1 h). Whilst this is a commonly used study design to robustly assess the rehydration efficacy of different beverages, future studies should distribute fluid intake over a longer duration, in order to improve ecological validity and reduce the risk of gastrointestinal issues.
Abstract licence: CC BY
Ford S, La Caze A, Coombes I, et al.
2026
- Hypoglycemia
- Hyperkalemia
- Insulin
BackgroundHyperkalaemia is a life-threatening electrolyte abnormality commonly managed with intravenous insulin-dextrose therapy (IDT). Although effective, IDT frequently causes hypoglycaemia, particularly in patients without diabetes. Glucose-only therapy, which leverages endogenous insulin production, may offer comparable potassium-lowering effects with reduced hypoglycaemia risk. However, evidence remains limited.MethodsThe HIGH-K Trial is a single-centre, double-blind, randomised controlled trial in adult, non-diabetic patients presenting to an Australian Emergency Department with hyperkalaemia (>5.5 mmol/L [99 mg/dL]). Ninety-five participants are randomised 1:1 to receive either glucose-only therapy (100 mL 50% dextrose bolus followed by 250 mL 10% dextrose infusion over 2 h) or standard IDT (10 units IV insulin with 25 g dextrose followed by 250 mL saline infusion). The primary safety outcome is the incidence of hypoglycaemia (DiscussionThis is the first double-blind, randomised controlled trial to directly compare the safety and biochemical non-inferiority of glucose-only therapy versus standard insulin-dextrose therapy in the emergency department. By utilising a continuous glucose infusion following a bolus, the protocol aims to sustain endogenous insulin release and optimise intracellular potassium shift while preventing hypoglycaemia. If non-inferiority is demonstrated, this approach could provide a safer alternative in high-acuity or resource-limited clinical settings.ConclusionResults will be disseminated in peer-reviewed journals and at national and international conferences. Findings may inform future research and clinical practice guidelines regarding glucose-only therapy for hyperkalaemia.
Abstract licence: CC BY
M. Walser
The American journal of physiology, 1961
W.F. Wonderlin, J.S. Strobl
Journal of Membrane Biology, 1996
F. M. Trefz, P. Constable, I. Lorenz
Journal of Veterinary Internal Medicine, 2017
Kataoka H
2026
Most studies of heart failure (HF) syndromes have focused on fluid regulation, particularly the balance of sodium and water. Approximately 10 years ago, in 2017, the "chloride theory" was proposed as a unifying hypothesis, suggesting that changes in serum chloride concentration are associated with shifts in plasma volume, hemodynamics, and neurohormonal activity during HF progression and treatment. This narrative review updates the chloride theory based on emerging clinical evidence. It further examines diuretic classification from a chloride-centered perspective, recent advances in guideline-directed medical therapy, and the potential role of chloride in loop diuretic resistance and its management. In addition, the review summarizes the prognostic relevance of changes in serum chloride during acute HF and the distinct pathophysiologic roles of sodium and chloride. Overall, this review provides an integrated perspective on HF pathophysiology, therapeutic strategies, and clinical monitoring within a chloride-centered framework.
Abstract licence: CC BY-NC
Sources: aggregated from Europe PMC (EMBL-EBI), OpenAlex, Crossref, PubMed and other open scholarly databases. Retracted articles are excluded. Study information is provided for research purposes and does not constitute medical advice.
Scientific data (pharmacology, interactions, ADME) is not yet available for this medicine. Clinical sections are sourced from the NHS dm+d database.