Potassium chloride 0.3% (potassium 40mmol/1litre) / Glucose 5% infusion 1litre polyethylene bottles
Requires a prescription from a doctor or prescriber
A white crystal or crystalline powder used as an electrolyte replenisher, in the treatment of hypokalemia, in buffer solutions, and in fertilizers and explosives.
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Potassium chloride 0.3% (potassium 40mmol/1litre) / Glucose 5% infusion 1litre polyethylene bottles
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.
NHS prescribing volume and spending trends
Guidelines from the National Institute for Health and Care Excellence
NICE clinical guidance(8)
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)
Patiromer for treating hyperkalaemia (TA623)
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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Pharmacy links redirect to the retailer's own search and do not represent real-time stock levels. Shortage and safety information sourced from MHRA drug safety updates (gov.uk, Crown Copyright under OGL v3.0).
Codes for healthcare professionals and prescribing systems
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NHS UK identifiers
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SNOMED CT and dm+d codes from NHS TRUD (Technology Reference data Update Distribution), licensed under the Open Government Licence v3.0. ATC codes from the WHO Collaborating Centre for Drug Statistics Methodology (whocc.no).
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: 11 · 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
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
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
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
C. Ellenberger, T. Sologashvili, Lukas Kreienbühl, et al.
Anesthesia & Analgesia, 2018
Jon F. Scott, Gina M. Robinson, Joyce M. French, et al.
Stroke, 1999
W.F. Wonderlin, J.S. Strobl
Journal of Membrane Biology, 1996
F. M. Trefz, P. Constable, I. Lorenz
Journal of Veterinary Internal Medicine, 2017
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.
Pharmacology and chemical data from DrugBank
Key facts
Drug status
Approved
Major interactions
None known
Half-life
Not available
Mechanism
Supplemental potassium in the form of high potassium food or potassium chloride…
Food interactions
2 warnings
Human targets
6 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
Elimination
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
The FDA withdrew its approval for the use of all solid oral dosage form drug products containing potassium chloride that supply 100 mg or more of potassium per dosage unit, except for controlled-release dosage forms and those products formulated for preparation of solution prior to ingestion.[L43942]
Known interactions with other medicines. Always consult a healthcare professional.
Showing 50 of 955 interactions
Late manifestations include muscle paralysis and cardiovascular collapse from cardiac arrest (9-12 mEq/L).
How the body processes this drug — absorption, distribution, metabolism, and elimination
Proteins and enzymes this drug interacts with in the body
PMID:16669787 PMID:32081947 PMID:32294086 PMID:33597714 PMID:35585053 PMID:36239040 PMID:36306358 PMID:7629105
Plays a vital role in the regulation of ionic balance and cell volume PMID:16669787 PMID:32081947 PMID:32294086 PMID:7629105
PMID:21321328
Electrically silent transporter system (By similarity)
PMID:12106695
As major extruder of intracellular chloride, it establishes the low neuronal Cl(-) levels required for chloride influx after binding of GABA-A and glycine to their receptors, with subsequent hyperpolarization and neuronal inhibition (By similarity). Involved in the regulation of dendritic spine formation and maturation PMID:24668262
PMID:10600773 PMID:11551954 PMID:16048901 PMID:18566107 PMID:19665974 PMID:21628467 PMID:27485015
May contribute to cell volume homeostasis in single cells PMID:16048901 PMID:27485015
PMID:10913127
May mediate K(+) uptake into Deiters' cells in the cochlea and contribute to K(+) recycling in the inner ear. Important for the survival of cochlear outer and inner hair cells and the maintenance of the organ of Corti. May be required for basolateral Cl(-) extrusion in the kidney and contribute to renal acidification (By similarity)
Proteins that transport this drug across cell membranes
PMID:16669787 PMID:32081947 PMID:32294086 PMID:33597714 PMID:35585053 PMID:36239040 PMID:36306358 PMID:7629105
Plays a vital role in the regulation of ionic balance and cell volume PMID:16669787 PMID:32081947 PMID:32294086 PMID:7629105
PMID:21321328
Electrically silent transporter system (By similarity)
PMID:12106695
As major extruder of intracellular chloride, it establishes the low neuronal Cl(-) levels required for chloride influx after binding of GABA-A and glycine to their receptors, with subsequent hyperpolarization and neuronal inhibition (By similarity). Involved in the regulation of dendritic spine formation and maturation PMID:24668262
PMID:10600773 PMID:11551954 PMID:16048901 PMID:18566107 PMID:19665974 PMID:21628467 PMID:27485015
May contribute to cell volume homeostasis in single cells PMID:16048901 PMID:27485015
PMID:10913127
May mediate K(+) uptake into Deiters' cells in the cochlea and contribute to K(+) recycling in the inner ear. Important for the survival of cochlear outer and inner hair cells and the maintenance of the organ of Corti. May be required for basolateral Cl(-) extrusion in the kidney and contribute to renal acidification (By similarity)
PMID:35759661
May contribute to cell volume homeostasis in single cells .
PMID:10913127 PMID:34031912
May be involved in the regulation of basolateral Cl(-) exit in NaCl absorbing epithelia (By similarity)
ATC B05XA01
ATC A12BA01
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
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Chemical identifiers
CAS, UNII, InChI Key and database cross-references
DrugBank citations
If you use DrugBank data in your research, please cite:
- DrugBank 6.02024Recommended citationKnox C., Wilson M., Klinger C.M., et alDrugBank 6.0: the DrugBank Knowledgebase for 2024Nucleic Acids Res. 2024 Jan 552(D1):D1265-D1275
- DrugBank 5.02018Wishart D.S., Feunang Y.D., Guo A.C., et alDrugBank 5.0: a major update to the DrugBank database for 2018Nucleic Acids Res. 2017 Nov 846(D1):D1074-D1082
- DrugBank 4.02014Law V., Knox C., Djoumbou Y., et alDrugBank 4.0: shedding new light on drug metabolismNucleic Acids Res. 2014 Jan 142(1):D1091-7
- DrugBank 3.02011Knox C., Law V., Jewison T., et alDrugBank 3.0: a comprehensive resource for 'omics' research on drugsNucleic Acids Res. 2011 Jan39(Database issue):D1035-41
- DrugBank 2.02008Wishart D.S., Knox C., Guo A.C., et alDrugBank: a knowledgebase for drugs, drug actions and drug targets.Nucleic Acids Research2008 Jan36(Database issue):D901-6
- DrugBank 1.02006Wishart D.S., Knox C., Guo A.C., et alDrugBank: a comprehensive resource for in silico drug discovery and exploration.Nucleic Acids Research2006 Jan 134(Database issue):D668-72