Potassium citrate
Regulatory sources consulted
Approved indications
- Management of renal tubular acidosis with calcium stones, hypocitraturic calcium oxalate nephrolithiasis and uric-acid lithiasis with or without calcium stones.
Contraindications
Absolute
- Hyperkalaemia or conditions predisposing to hyperkalaemia.
- Delayed or arrested tablet transit, including delayed gastric emptying, oesophageal compression, intestinal obstruction or stricture, or anticholinergic use.
- Peptic-ulcer disease, active urinary-tract infection or renal impairment with glomerular filtration below 0.7 mL/kg/min.
Clinical warnings
- Major warning · It may cause rapidly developing, asymptomatic, life-threatening hyperkalaemia and cardiac arrest. Avoid when potassium excretion is impaired and monitor potassium and ECG. — https://api.fda.gov/drug/label.json?search=id:%229452b641-6fc4-444b-ba7e-f6a22430ba28%22&limit=1
- Major warning · If severe vomiting, abdominal pain or gastrointestinal bleeding occurs, stop immediately and investigate intestinal perforation or obstruction. — https://api.fda.gov/drug/label.json?search=id:%229452b641-6fc4-444b-ba7e-f6a22430ba28%22&limit=1
Drug interactions
- HighPotassium-sparing diureticsC03D
Mechanism: Simultaneous administration may cause severe hyperkalaemia.
Recommendation: Avoid concomitant administration.
https://api.fda.gov/drug/label.json?search=id:%229452b641-6fc4-444b-ba7e-f6a22430ba28%22&limit=1
- HighDrugs that slow gastrointestinal transit, such as anticholinergics
Mechanism: They may increase gastrointestinal irritation from potassium salts and delay tablet transit.
Recommendation: Avoid this extended-release formulation when gastrointestinal transit is slowed.
https://api.fda.gov/drug/label.json?search=id:%229452b641-6fc4-444b-ba7e-f6a22430ba28%22&limit=1
- HighRenin-angiotensin-aldosterone system inhibitorsC09
Mechanism: They cause potassium retention and increase the risk of hyperkalaemia.
Recommendation: Closely monitor potassium during coadministration.
https://api.fda.gov/drug/label.json?search=id:%229452b641-6fc4-444b-ba7e-f6a22430ba28%22&limit=1
- ModerateNonsteroidal anti-inflammatory drugsM01A
Mechanism: They may cause potassium retention by reducing renal prostaglandin synthesis and impairing the renin-angiotensin system.
Recommendation: Closely monitor potassium during coadministration.
https://api.fda.gov/drug/label.json?search=id:%229452b641-6fc4-444b-ba7e-f6a22430ba28%22&limit=1
Adverse events
Common (≥1%)
Abdominal discomfort · Nausea · Vomiting · Diarrhoea or loose stools
Rare but serious
Hyperkalaemia and cardiac arrest · Gastrointestinal bleeding, perforation or obstruction
Pregnancy and lactation
FDA category: Solo si es claramente necesario
During pregnancy, use only if clearly needed. During breastfeeding, it is unknown whether it alters the normal potassium content of human milk; use only if clearly needed.
Recent literature (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