Potassium citrate mixture
Available from a pharmacy with pharmacist advice
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MHRA alerts for Potassium citrate + Citric acid
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Potassium citrate mixture
Potassium citrate mixture
This is the NHS Drug Tariff indicative price used for reimbursement purposes. It may not reflect the price paid by patients or pharmacies.
View full Drug TariffSource: NHS Drug Tariff via NHSBSA. Derived from dm+d VMPP (Virtual Medicinal Product Pack) pricing data. Contains public sector information licensed under the Open Government Licence v3.0.
WHO defined daily dose (DDD)
4 gram
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.
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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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 27 studies.
Reviews & meta-analyses: 1 · Randomised trials: 1 · 1943–2026
Showing all 27 studies, sorted by most relevant.
Li P, Yang X, Lang Y, et al.
2025
- Calcium Oxalate
- Hydrogen-Ion Concentration
- Kidney Calculi
P.A. Srere
Methods in Enzymology, 1969
Seema Gosavi, Rushikesh Nanaware
Asian Journal of Pharmaceutical Analysis, 2024
Yoshiro Takeda, Fujio Suzuki, Hideo Inoue
Methods in Enzymology, 1969
Kongjie Wu, Chengxiao Hu, Yuqing Duan, et al.
Journal of agricultural and food chemistry, 2025
- Potassium
- Vacuoles
- Citric Acid
J. Loutit, P. Mollison, I. M. Young, et al.
Experimental Physiology, 1943
Zomorodian A, Moe OW
2025
Citrate, a tricarboxylic acid cycle intermediate, plays a central role in renal physiology by acting as both a urinary base equivalent and a potent inhibitor of calcium stone formation. Hypocitraturia, a common metabolic abnormality in calcium nephrolithiasis, is not a binary disorder but a continuum shaped by acid-base status, diet, potassium balance, proximal tubular handling, and systemic citrate status. We provide an update on the biology of citrate, renal regulation of its excretion, clinical pathophysiology, and treatment of hypocitraturia. Identical urinary citrate levels may have different implications depending on systemic acid-base status and urinary calcium excretion. Hypocitraturia prevalence is increasing, paralleling rises in metabolic syndrome, obesity, and dietary habit changes. Experimental models confirm that systemic or intracellular acidosis, potassium deficiency, and upregulation of renal transport and metabolism of citrate reduce urinary citrate, enhancing stone risk. Potassium citrate remains the cornerstone of therapy, increasing both urinary citrate and pH. However, its use requires caution in calcium phosphate stone formers and patients with chronic kidney disease. Citrate resistance, defined as inadequate urinary citrate response despite good potassium delivery, is a therapeutic challenge. Novel interventions including sodium-dicarboxylate cotransporter-1 (NaDC-1) inhibitors and citrate analogs such as hydroxycitrate may offer future alternatives. In conclusion, urinary citrate must be interpreted within physiological and clinical contexts. Recognizing hypocitraturia as a modifiable, non-binary risk factor allows for more precise risk stratification and individualized therapy in stone prevention, particularly when lithogenicity overlaps with acid-base and renal abnormalities.
Abstract licence: CC BY
S. Doizi, J. Poindexter, M. Pearle, et al.
The Journal of urology, 2018
- Calcium Phosphates
- Placebos
- Urinary Calculi
T. Maltseva
Ukrainian Chemistry Journal, 2025
Kitamura W, Fujii K, Abe M, et al.
2025
- Peripheral Blood Stem Cells
- Sodium Citrate
- Glucose
BACKGROUND: As the processed blood volume increases, a larger amount of anticoagulant (AC) is required, which leads to a serious issue of fluid dilution in large-volume leukocytapheresis (defined as ≥3-fold total blood volume). We previously reported a novel method for allogeneic peripheral blood stem cell harvest (PBSCH) using highly concentrated sodium citrate (HSC; 5.32%), which shortened the procedure time and reduced the need for an AC solution without heparin. In this study, we extended this novel method to autologous PBSCH (auto-PBSCH) and compared it with patients who received auto-PBSCH using normal concentrated sodium citrate (NSC; 2.2%). STUDY DESIGN AND METHODS: We retrospectively analyzed consecutive auto-PBSCH data obtained using the Spectra Optia continuous mononuclear cell collection mode between May 2017 and May 2025 at our institution. RESULTS: Leukocytapheresis was performed using NSC in 36 patients and HSC in 22. In the HSC group, patients tended to be younger, had significantly lower body weight, and had significantly fewer hematopoietic tumors as primary diseases compared to the NSC group. After propensity score-matched cohort adjusted for patient background, the total amount of AC solution was significantly lower (694 [range, 77-1648] vs. 298 mL [range, 64-797], p = .02), and procedure time was significantly shorter (224 [range, 117-395] vs. 181 min [range, 103-309], p = .048) in the HSC group. Furthermore, the loss rates of magnesium and potassium were lower in the HSC group. CONCLUSION: This novel leukocytapheresis method demonstrated the efficacy and safety in auto-PBSCH, while minimizing the patient burden.
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.
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Linked open data from Wikidata (Q419921), a free and open knowledge base operated by the Wikimedia Foundation. Data is available under the Creative Commons CC0 1.0 Public Domain Dedication. WHO INN from the World Health Organization.
Scientific data (pharmacology, interactions, ADME) is not yet available for this medicine. Clinical sections are sourced from the NHS dm+d database.