Potassium citrate
Sources réglementaires consultées
Indications approuvées
- Traitement de l'acidose tubulaire rénale avec calculs calciques, de la néphrolithiase oxalocalcique avec hypocitraturie et de la lithiase urique avec ou sans calculs calciques.
Contre-indications
Absolues
- Hyperkaliémie ou affections prédisposant à l'hyperkaliémie.
- Retard ou arrêt du transit du comprimé, notamment retard de la vidange gastrique, compression œsophagienne, obstruction ou sténose intestinale, ou utilisation d'anticholinergiques.
- Ulcère gastroduodénal, infection urinaire active ou insuffisance rénale avec filtration glomérulaire inférieure à 0,7 ml/kg/min.
Mises en garde cliniques
- Mise en garde majeure · Il peut provoquer une hyperkaliémie potentiellement mortelle et un arrêt cardiaque, d'apparition rapide et asymptomatique. Éviter en cas d'altération de l'excrétion du potassium et surveiller le potassium et l'ECG. — https://api.fda.gov/drug/label.json?search=id:%229452b641-6fc4-444b-ba7e-f6a22430ba28%22&limit=1
- Mise en garde majeure · En cas de vomissements sévères, de douleur abdominale ou d'hémorragie digestive, arrêter immédiatement et rechercher une perforation ou une obstruction intestinale. — https://api.fda.gov/drug/label.json?search=id:%229452b641-6fc4-444b-ba7e-f6a22430ba28%22&limit=1
Interactions médicamenteuses
- SévèreDiurétiques épargneurs de potassiumC03D
Mécanisme: L'administration simultanée peut provoquer une hyperkaliémie sévère.
Recommandation: Éviter l'administration concomitante.
https://api.fda.gov/drug/label.json?search=id:%229452b641-6fc4-444b-ba7e-f6a22430ba28%22&limit=1
- SévèreMédicaments ralentissant le transit gastro-intestinal, tels que les anticholinergiques
Mécanisme: Ils peuvent augmenter l'irritation gastro-intestinale due aux sels de potassium et retarder le transit du comprimé.
Recommandation: Éviter cette formulation à libération prolongée lorsque le transit gastro-intestinal est ralenti.
https://api.fda.gov/drug/label.json?search=id:%229452b641-6fc4-444b-ba7e-f6a22430ba28%22&limit=1
- SévèreInhibiteurs du système rénine-angiotensine-aldostéroneC09
Mécanisme: Ils entraînent une rétention potassique et augmentent le risque d'hyperkaliémie.
Recommandation: Surveiller étroitement le potassium pendant l'administration concomitante.
https://api.fda.gov/drug/label.json?search=id:%229452b641-6fc4-444b-ba7e-f6a22430ba28%22&limit=1
- ModéréeAnti-inflammatoires non stéroïdiensM01A
Mécanisme: Ils peuvent entraîner une rétention potassique en réduisant la synthèse rénale des prostaglandines et en altérant le système rénine-angiotensine.
Recommandation: Surveiller étroitement le potassium pendant l'administration concomitante.
https://api.fda.gov/drug/label.json?search=id:%229452b641-6fc4-444b-ba7e-f6a22430ba28%22&limit=1
Effets indésirables
Communs (≥1%)
Gêne abdominale · Nausées · Vomissements · Diarrhée ou selles molles
Rares mais graves
Hyperkaliémie et arrêt cardiaque · Hémorragie, perforation ou obstruction gastro-intestinale
Grossesse et allaitement
Catégorie FDA: Solo si es claramente necesario
Pendant la grossesse, utiliser uniquement en cas de nécessité clairement établie. Pendant l'allaitement, on ignore si le produit modifie la teneur normale en potassium du lait humain ; utiliser uniquement en cas de nécessité clairement établie.
Bibliographie récente (PubMed)
Kidney stone disease is rapidly increasing with a strong relationship to metabolic syndrome. This review gives a brief overview of the current state and current treatment modalities. Increasing use of CT and ultrasound scans leads to increased diagnosis of asymptomatic kidney stones, which rarely require treatment. The trend in stone treatment goes towards endoscopic lithotripsy which together with ESWL enables a personalised approach. Obstructive stones with infection require urgent intervention to reduce mortality. Increased fluid intake, dietary changes as well as potassium citrate supplements are the most important elements in stone prevention in the common idiopathic stone disease. Kidney stones are concretions of different mineral salts mixed with an organic matrix that form in the upper urinary tract. As a stone moves from the kidney to the ureter, it can present with renal colic symptoms and may cause urinary tract obstruction and/or infection. In fact, acute passage of a kidney stone is one of the leading reasons for visits to an emergency room. Over the past four decades, the lifetime prevalence of nephrolithiasis has more than doubled in the United States (and several other developed countries), afflicting around 11% of men and 7% of women. Unless the underlying etiology of stone formation is adequately addressed, kidney stones can recur at a rate of around 50% ten years after initial presentation. The evaluation of a kidney stone former requires an extensive medical history (to identify environmental, metabolic, and/or genetic factors contributing to stone formation), imaging studies to evaluate and track stone burden, and laboratory studies (serum and urinary chemistries, stone composition analysis) to guide lifestyle and pharmacological therapy. The majority of kidney stones are composed of calcium (calcium oxalate and/or calcium phosphate), either pure or in combination with uric acid. Calcium oxalate stones can be caused by hypercalciuria, hyperoxalu
The formation of kidney stones is a complex biologic process involving interactions among genetic, anatomic, dietary, and environmental factors. Traditional lithogenic models were based on urine supersaturation in relation to the activity of crystallization promoters and inhibitors. However, modern research has added new principles such as the "renal epithelial cell response" and the role of inflammation and oxidative stress leading to the development of a "multi-hit hypothesis". A strong correlation between urinary stones and kidney damage has been well demonstrated by both cohort and case-control studies. The main contributors to chronic kidney damage associated with urinary stones include crystal deposition within the renal parenchyma, associated comorbidities, repeated obstructive and infectious episodes, as well as the potential adverse effects of stone removal procedures. Most hereditary stones may cause high urinary saturation levels promoting obstruction of the Bellini ducts and consequent glomerulosclerosis and interstitial fibrosis in the cortex. These include hereditary hypercalciurias, primary hyperoxalurias, cystinuria, adenine phosphoribosyltransferase (APRT) deficiency (associated with 2,8-dihydroxyadenine lithiasis) and xanthinuria. Complete distal renal tubular acidosis occurs in childhood and presents deafness, rickets, and a short life expectancy. The incomplete form usually manifests in adulthood, primarily with recurrent urinary lithiasis, and less frequently with nephrocalcinosis. In all stone formers stone analysis and a basic metabolic evaluation, including blood biochemistry, urine sediment examination, urinary pH and culture are mandatory, in contrast high-risk stone formers require a more specific metabolic evaluation, including a 24-hour urine sample to measure calcium, phosphate, citrate, oxalate, uric acid, magnesium, sodium and proteinuria. The morpho compositional analysis of kidney stones offers essential insights beyond merely ident