Furosemide 20mg / Potassium chloride 750mg (potassium 10mmol) modified-release tablets
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WHO defined daily dose (DDD)
40 mg
Not a recommended dose. The DDD is the assumed average maintenance dose per day for a drug used for its main indication in adults. It is a statistical measure used for research and comparison purposes only.
Source: WHO Collaborating Centre for Drug Statistics Methodology, distributed via the NHS dm+d supplementary BNF/ATC mapping files (NHSBSA). Contains public sector information licensed under the Open Government Licence v3.0.
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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. BNF code shown is the factual mapping value distributed by NHS Business Services Authority (NHSBSA) in the dm+d supplementary file under OGL v3.0; it is not affiliated with, nor licensed from, the publishers of the British National Formulary. 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 all 21 studies.
Reviews & meta-analyses: 1 · Randomised trials: 1 · 1980–2026
Showing all 21 studies, sorted by most relevant.
Bindal T, Sinha A, Yadav M, et al.
2026
- Torsemide
- Diuretics
- Edema
P. Dunham, G. Stewart, J. Ellory
Proceedings of the National Academy of Sciences of the United States of America, 1980
- Biological Transport
- Cell Membrane Permeability
- Chlorides
J. Russell
The Journal of General Physiology, 1983
J. Hennings, O. Andrini, N. Picard, et al.
Journal of the American Society of Nephrology : JASN, 2017
- Diuretics
- Furosemide
- Nephrons
Chloride transport by the renal tubule is critical for blood pressure (BP), acid-base, and potassium homeostasis. Chloride uptake from the urinary fluid is mediated by various apical transporters, whereas basolateral chloride exit is thought to be mediated by ClC-Ka/K1 and ClC-Kb/K2, two chloride channels from the ClC family, or by KCl cotransporters from the SLC12 gene family. Nevertheless, the localization and role of ClC-K channels is not fully resolved. Because inactivating mutations in ClC-Kb/K2 cause Bartter syndrome, a disease that mimics the effects of the loop diuretic furosemide, ClC-Kb/K2 is assumed to have a critical role in salt handling by the thick ascending limb. To dissect the role of this channel in detail, we generated a mouse model with a targeted disruption of the murine ortholog ClC-K2. Mutant mice developed a Bartter syndrome phenotype, characterized by renal salt loss, marked hypokalemia, and metabolic alkalosis. Patch-clamp analysis of tubules isolated from knockout (KO) mice suggested that ClC-K2 is the main basolateral chloride channel in the thick ascending limb and in the aldosterone-sensitive distal nephron. Accordingly, ClC-K2 KO mice did not exhibit the natriuretic response to furosemide and exhibited a severely blunted response to thiazide. We conclude that ClC-Kb/K2 is critical for salt absorption not only by the thick ascending limb, but also by the distal convoluted tubule.
Abstract licence: CC BY
A. Jaggi, Aalamjeet Kaur, Anjana Bali, et al.
Current Neuropharmacology, 2015
- Anticonvulsants
- Epilepsy
- Potassium Chloride
Sodium potassium chloride co-transporter (NKCC) belongs to cation-dependent chloride co-transporter family, whose activation allows the entry of Na(+), K(+) and 2Cl(-) inside the cell. It acts in concert with K(+) Cl(-) co-transporter (KCC), which extrudes K(+) and Cl(-) ions from cell. NKCC1 is widely distributed throughout the body, while NKCC2 is exclusively present in kidney. Protein kinase A, protein kinase C, Ste20-related proline-alanine-rich kinase, oxidative stress responsive kinases, With No K=lysine kinase and protein phosphatase type 1 control the phosphorylation/dephosphorylation of key threonine residues of in regulatory domain of NKCC1. The selective inhibitors of NKCC1 including bumetanide and furosemide are conventionally employed as diuretics. However, recent studies have indicated that NKCC1 may be involved in the pathophysiology of anxiety, cerebral ischemia, epilepsy, neuropathic pain, fragile X syndrome, autism and schizophrenia. The inhibitors of NKCC1 are shown to produce anxiolytic effects; attenuate cerebral ischemia-induced neuronal injury; produce antiepileptic effects and attenuate neuropathic pain. In the early developing brain, GABAA activation primarily produces excitatory actions due to high NKCC1/KCC2 ratio. However, as the development progresses, the ratio of NKCC1/KCC2 ratio reverses and there is switch in the polarity of GABAA actions and latter acquires the inhibitory actions. The recapitulation of developmental-like state during pathological state may be associated with increase in the expression and functioning of NKCC1, which decreases the strength of inhibitory GABAergic neurotransmission. The present review describes the expanding role and mechanism of NKCC1 in the pathophysiology of different diseases.
Abstract licence: CC BY
S. El-Guendouz, N. Al-Waili, Smail Aazza, et al.
Asian Pacific journal of tropical medicine, 2017
OBJECTIVE: To study the antioxidant properties of Capparis spinosa (C. spinosa) honey and propolis and the effect of combined honey and propolis administration on urine volume and electrolytes in rats. METHODS: C. spinosa honey [1000 mg/kg body weight (b.wt)], propolis (100 mg/kg b.wt), honey/propolis mixture (C. spinosa honey 1000 mg/kg b.wt/ propolis extract 100 mg/kg b.wt ), distilled water (1 mL/kg b.wt) and furosemide (10 mg/kg b.wt) were orally administered to five groups of rats for 21 d. Urine volume, blood and urine sodium, potassium and chloride were measured. The antioxidant activity of propolis and honey was assessed and their total phenols and flavonoids were determined. RESULTS: Propolis and C. spinosa honey contain polyphenols including flavonoids and propolis demonstrated higher antioxidant activities than honey. Honey significantly increased urine volume and urine electrolyte excretion. Propolis had no significant effect on urine volume, but co-administration of propolis and honey caused significant diuresis. No major changes were observed in plasma electrolytes with the use of honey, propolis or their combination. CONCLUSIONS: Honey and propolis have antioxidant activity and contain polyphenols including flavonoids that are more pronounced in propolis. Honey has a significant diuretic activity alone or in combination with propolis. This is the first study comparing the diuretic effect of co-administration of propolis and C. spinosa honey with furosemide.
Abstract licence: CC BY-NC-ND
H. Pasantes‐morales, R. A. Murray, L. Lilja, et al.
The American journal of physiology, 1994
- K Cl- Cotransporters
- Anions
- Astrocytes
T. Nelin, Matthew Huber, Erik A. Jensen, et al.
Journal of perinatology : official journal of the California Perinatal Association, 2024
- Bronchopulmonary Dysplasia
- Chlorides
- Chlorothiazide
OBJECTIVES: To examine the association of novel furosemide versus thiazide diuretic exposure with changes in serum sodium, potassium, and chloride levels among infants with grade 2/3 bronchopulmonary dysplasia (BPD). STUDY DESIGN: Retrospective cohort study of infants admitted to a level IV neonatal intensive care unit (NICU) with grade 2/3 BPD. We measured within-subject change in serum sodium, potassium, and chloride before and after diuretic initiation using multivariable regression to adjust for differences in dosing and clinical covariates. RESULTS: We identified 94 infants contributing 137 novel diuretic exposures. No significant difference was noted in the association between chlorothiazide versus furosemide and serum sodium, potassium, or chloride change in multivariable modeling. CONCLUSIONS: Changes in serum electrolytes were similar for chlorothiazide and furosemide, questioning the perception that chlorothiazide leads to less electrolyte derangement among preterm infants with grade 2/3 BPD.
Abstract licence: CC BY
Tbatou W, Aboulghazi A, El Ghouizi A, et al.
2025
Objective: bark ethanolic extract (PPBE). Materials and Methods: The phytochemical composition of PPBE was assessed using HPLC-DAD. Total polyphenols and flavonoids were quantified using the Folin-Ciocalteu and aluminum trichloride methods, respectively, while mineral content was determined by plasma mass spectrometry. Antioxidant activity was assessed using the reducing power assay, total antioxidant capacity, and anti-DPPH free radical assay. For the diuretic effect, sixteen male Wistar rats were divided into four groups: control (distilled water, 10 ml/kg of BW), furosemide (10 mg/kg of BW), and PPBE (200 and 400 mg/kg of BW) groups. After 15 days, plasma and urine were collected for creatinine, potassium, and sodium analysis, along with urine output measurement. Statistical analysis employed one-way ANOVA followed by Tukey multiple comparison test. Results: The PPBE displayed high phenolic content and potent antioxidant properties. Besides, the PPBE phenolic screening showed nine phenolic compounds with ferulate glucoside, gallic acid, and catechin as the main compounds. The PPBE demonstrated a richness in essential minerals. Furthermore, at both doses (200 and 400 mg/kg) PPBE led to a notable elevation in urine flow, urinary sodium concentration, and creatinine clearance, without affecting plasma electrolytes. In contrast, furosemide caused a reduction in plasma potassium levels. Conclusion: PPBE could serve as a bioactive component, antioxidant, or preservative in food formulation. Moreover, it exhibits a diuretic effect without altering plasma composition.
Abstract licence: CC BY
Boosman RJ, Chan RM, Nur E, et al.
2026
- Cyclophosphamide
- Cystitis
- Fluid Therapy
Abstract Purpose Cyclophosphamide is a commonly used chemotherapeutic agent in hematopoietic stem cell transplantation (HSCT), but its use can lead to adverse effects such as hemorrhagic cystitis (HC) and electrolyte disturbances, including hyponatremia. While standard hydration protocols are used to mitigate these risks, the optimal regimen remains unclear. This study explores the impact of a restrictive hydration regimen on HC incidence and electrolyte imbalances in patients undergoing high-dose cyclophosphamide treatment as part of HSCT conditioning. Methods A retrospective cohort study was conducted at Amsterdam UMC, including patients who received high-dose cyclophosphamide as part of HSCT between 2016 and 2024. Patients were grouped based on hydration protocols: an original regimen (5 L of NaCl 0.45%/dextrose 2.5% per day) and a new restrictive regimen (1.5 L/m 2 /day of 0.65% NaCl). The primary endpoint was the incidence of HC, while secondary endpoints included sodium and potassium changes, fluid overload (measured by furosemide use), and clinical outcomes. Results HC occurred in 10/386 (2.6%) patients in the original protocol and 1/69 (1.4%) in the restrictive protocol (odds ratio [95% confidence interval]: 0.55 [0.03–2.96], p = 0.57). Clinically relevant hyponatremia was less common with the restrictive regimen (1.4%) than with the original protocol (4.4%), though the difference was not significant ( p = 0.27). On the other hand, patients receiving the restrictive regimen showed more clinically relevant hypokalemia (8.7% vs 5.9%, p = 0.28). Fluid overload, as indicated by furosemide use, was lower in the restrictive group albeit not statistically significant. Conclusion In this retrospective single-center cohort, we did not observe a higher incidence of HC or electrolyte imbalances with a restrictive hydration regimen compared to the original regimen.
Abstract licence: CC BY
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.