TASCIT Potassium Citrate 1620mg (Eq. 15mEq) Extended-Release Tablet 1's
RXDRUG-DR-XY44622-1pc
Discreet Packaging
FDA-registered Products
FDA-licensed Pharmacies
Indications/Uses
For the management of: Renal tubular acidosis (RTA) with calcium stones; Hypocitraturic calcium oxalate nephrolithiasis of any etiology; Uric acid lithiasis with or without calcium stones.
For the prevention of stone relapse after extracorporeal shock wave lithotripsy (ESWL) or lithotomy
For the prevention of stone relapse after extracorporeal shock wave lithotripsy (ESWL) or lithotomy
Dosage/Direction for Use
General Dosing Recommendations: Potassium citrate extended-release tablet is in a wax matrix slow-release preparation. The tablet should be swallowed whole, not crushed, chewed or sucked to prevent premature release of active ingredient.
Take the tablet 30 minutes after meals.
Limit salt intake by avoiding food with high salt content while on potassium citrate therapy.
Increase fluid intake. Urine volume should be at least two liters per day.
Adult Dose: Severe Hypocitraturia (urinary citrate <150 mg/day): Orally, 60 mEq/day taken in two or three divided doses (30 mEq two times/day or 20 mEq three times/day).
Mild to Moderate Hypocitraturia (urinary citrate >150 mg/day): Orally, 30 mEq/day taken in two or three divided doses (15 mEq two times/day or 10 mEq three times/day).
Or, as prescribed by a physician.
Take the tablet 30 minutes after meals.
Limit salt intake by avoiding food with high salt content while on potassium citrate therapy.
Increase fluid intake. Urine volume should be at least two liters per day.
Adult Dose: Severe Hypocitraturia (urinary citrate <150 mg/day): Orally, 60 mEq/day taken in two or three divided doses (30 mEq two times/day or 20 mEq three times/day).
Mild to Moderate Hypocitraturia (urinary citrate >150 mg/day): Orally, 30 mEq/day taken in two or three divided doses (15 mEq two times/day or 10 mEq three times/day).
Or, as prescribed by a physician.
Overdosage
Overdosage with potassium salts may cause hyperkalemia and alkalosis, especially in the presence of renal disease. It is necessary to recognize that hyperkalemia is usually asymptomatic and may be manifested only by an increased serum potassium concentration and characteristic electrocardiographic changes (peaking T-wave, loss of P-wave, depression of S-T segment and prolongation of the QT interval). Late manifestations include muscle paralysis and cardiovascular collapse from cardiac arrest.
Measures for treating hyperkalemia include the following: Patients should be closely monitored for arrhythmias and electrolyte changes.
Elimination of potassium-containing medications and of agents with potassium sparing properties such as potassium-sparing diuretics, angiotensin receptor blockers (ARBs), angiotensin converting enzyme (ACE) inhibitors, nonsteroidal anti-inflammatory drugs (NSAIDs), certain nutritional supplements and many others.
Elimination of foods containing high levels of potassium such as almonds, bananas, beans, grapefruit juice, halibut, milk, salmon, spinach, tuna and many others.
Intravenous calcium gluconate if the patient is at no risk or low risk of developing digitalis toxicity.
Intravenous administration of 300 to 500 mL/hr of 10% dextrose solution containing 10 to 20 units of crystalline insulin per 1000 mL.
Correction of acidosis, if present, with intravenous sodium bicarbonate.
Hemodialysis or peritoneal dialysis.
Exchange resins may be used. However, this measure alone is not sufficient for the acute treatment of hyperkalemia.
Lowering potassium levels too rapidly in patients taking digitalis can produce digitalis toxicity.
Measures for treating hyperkalemia include the following: Patients should be closely monitored for arrhythmias and electrolyte changes.
Elimination of potassium-containing medications and of agents with potassium sparing properties such as potassium-sparing diuretics, angiotensin receptor blockers (ARBs), angiotensin converting enzyme (ACE) inhibitors, nonsteroidal anti-inflammatory drugs (NSAIDs), certain nutritional supplements and many others.
Elimination of foods containing high levels of potassium such as almonds, bananas, beans, grapefruit juice, halibut, milk, salmon, spinach, tuna and many others.
Intravenous calcium gluconate if the patient is at no risk or low risk of developing digitalis toxicity.
Intravenous administration of 300 to 500 mL/hr of 10% dextrose solution containing 10 to 20 units of crystalline insulin per 1000 mL.
Correction of acidosis, if present, with intravenous sodium bicarbonate.
Hemodialysis or peritoneal dialysis.
Exchange resins may be used. However, this measure alone is not sufficient for the acute treatment of hyperkalemia.
Lowering potassium levels too rapidly in patients taking digitalis can produce digitalis toxicity.
Administration
Should be taken with food: Take 30 min after meals. Swallow whole, do not crush/chew/suck.
Contraindications
Hypersensitivity to any component of the product.
Patients with hyperkalemia or who have conditions predisposing them to hyperkalemia such as: Chronic renal failure; Uncontrolled diabetes mellitus; Familial hyperkalemic periodic paralysis (adynamia episodica hereditaria); Acute dehydration; Strenuous physical exercise in unconditioned individuals; Adrenal insufficiency; Extensive tissue breakdown; Severe myocardial damage; Administration of potassium-sparing diuretic (e.g., triamterene, spironolactone or amiloride).
Patients with slow gastric emptying, esophageal compression, intestinal obstruction or stricture.
Patients on anticholinergic therapy.
Patients with active peptic ulcer disease.
Patients with active urinary tract infection (with either urea-splitting bacteria or other organisms, in association with either calcium or struvite stones).
Patients with renal insufficiency (glomerular filtration rate of less than 0.7 mL/kg/min).
Patients with respiratory or metabolic acidosis.
Patients with hyperkalemia or who have conditions predisposing them to hyperkalemia such as: Chronic renal failure; Uncontrolled diabetes mellitus; Familial hyperkalemic periodic paralysis (adynamia episodica hereditaria); Acute dehydration; Strenuous physical exercise in unconditioned individuals; Adrenal insufficiency; Extensive tissue breakdown; Severe myocardial damage; Administration of potassium-sparing diuretic (e.g., triamterene, spironolactone or amiloride).
Patients with slow gastric emptying, esophageal compression, intestinal obstruction or stricture.
Patients on anticholinergic therapy.
Patients with active peptic ulcer disease.
Patients with active urinary tract infection (with either urea-splitting bacteria or other organisms, in association with either calcium or struvite stones).
Patients with renal insufficiency (glomerular filtration rate of less than 0.7 mL/kg/min).
Patients with respiratory or metabolic acidosis.
Special Precautions
Hyperkalemia: Potassium citrate administration can produce hyperkalemia and cardiac arrest in patients with impaired mechanisms for potassium excretion. Potentially fatal hyperkalemia may develop rapidly and may be asymptomatic. Use of potassium citrate should therefore be avoided in patients with chronic renal failure, or any other condition which impairs potassium excretion such as severe myocardial damage or heart failure.
Gastrointestinal Lesions: In the event of severe vomiting, abdominal pain or gastrointestinal bleeding, potassium citrate treatment should be discontinued immediately and the possibility of bowel perforation or obstruction investigated. Patient should also be instructed to inform physician at once if tarry stools or other evidence of gastrointestinal bleeding is noticed.
General: Regular serum potassium monitoring is recommended. Acid-base balance, other serum electrolyte levels, and electrocardiogram (ECG) should periodically be determined. Careful attention should likewise be given to the patient's clinical status, particularly in the presence of cardiac disease, renal disease or acidosis.
Discontinue potassium citrate treatment in the occurrence of hyperkalemia, a significant rise in serum creatinine, or a significant fall in blood hematocrit or hemoglobin.
Use in Children: Safety and efficacy in children have not been established.
Gastrointestinal Lesions: In the event of severe vomiting, abdominal pain or gastrointestinal bleeding, potassium citrate treatment should be discontinued immediately and the possibility of bowel perforation or obstruction investigated. Patient should also be instructed to inform physician at once if tarry stools or other evidence of gastrointestinal bleeding is noticed.
General: Regular serum potassium monitoring is recommended. Acid-base balance, other serum electrolyte levels, and electrocardiogram (ECG) should periodically be determined. Careful attention should likewise be given to the patient's clinical status, particularly in the presence of cardiac disease, renal disease or acidosis.
Discontinue potassium citrate treatment in the occurrence of hyperkalemia, a significant rise in serum creatinine, or a significant fall in blood hematocrit or hemoglobin.
Use in Children: Safety and efficacy in children have not been established.
Use In Pregnancy & Lactation
Pregnancy: Pregnancy Category C. It is not known whether potassium citrate can cause fetal harm when administered to a pregnant woman or can affect reproductive capacity. Potassium citrate should be given to a pregnant woman only if clearly needed.
Lactation: The normal potassium ion content of human milk is about 13 mEq/L; it is not known if potassium citrate has an effect on the milk potassium content. Exercise caution when potassium citrate is administered to a breastfeeding woman.
Lactation: The normal potassium ion content of human milk is about 13 mEq/L; it is not known if potassium citrate has an effect on the milk potassium content. Exercise caution when potassium citrate is administered to a breastfeeding woman.
Adverse Reactions
Potassium citrate therapy may cause minor gastrointestinal complaints such as abdominal discomfort, vomiting, diarrhea, loose bowel movements, and nausea. These symptoms are due to irritation of the gastrointestinal tract, and may be avoided by taking the dose with meals or snack, or dose reduction. Intact matrices may appear in the feces.
Drug Interactions
Potassium-sparing Diuretics: Concomitant administration of potassium citrate and potassium-sparing diuretics (e.g., triamterene, spironolactone, or amiloride) should be avoided, since simultaneous administration of these agents can produce severe hyperkalemia.
Drugs that slow gastrointestinal transit time: These agents (e.g., anticholinergics) can be expected to increase the gastrointestinal irritation caused by potassium salts.
Drugs that slow gastrointestinal transit time: These agents (e.g., anticholinergics) can be expected to increase the gastrointestinal irritation caused by potassium salts.
Storage
Store at temperatures not exceeding 30°C.
Action
Pharmacology: Pharmacodynamics: Metabolism of absorbed potassium citrate produces an alkaline load, raising urinary pH and increasing urinary citrate by augmenting citrate clearance. Thus, potassium citrate therapy appears to increase urinary citrate mainly by changing the renal handling of citrate, and, to a smaller extent, by increasing the filterable load of citrate. Increased urinary citrate and pH decrease calcium ion activity by increasing calcium complexation to dissociated anions and thus decreasing the saturation of calcium oxalate.
Potassium citrate also inhibits the crystallization and spontaneous nucleation of calcium oxalate and calcium phosphate in hypocitraturic calcium nephrolithiasis. However, potassium citrate does not alter the urinary saturation of calcium phosphate, because the effect of increased citrate complexation of calcium is antagonized by the rise in pH-dependent dissociation of phosphate. Calcium phosphate stones are more stable in alkaline urine.
Pharmacokinetics: Potassium citrate is oxidized in the body to form potassium bicarbonate. Oxidation is virtually complete. Less than 5% of the citrate is excreted unchanged in the urine.
Potassium citrate also inhibits the crystallization and spontaneous nucleation of calcium oxalate and calcium phosphate in hypocitraturic calcium nephrolithiasis. However, potassium citrate does not alter the urinary saturation of calcium phosphate, because the effect of increased citrate complexation of calcium is antagonized by the rise in pH-dependent dissociation of phosphate. Calcium phosphate stones are more stable in alkaline urine.
Pharmacokinetics: Potassium citrate is oxidized in the body to form potassium bicarbonate. Oxidation is virtually complete. Less than 5% of the citrate is excreted unchanged in the urine.
MedsGo Class
Other Drugs Acting on the Genito-Urinary System
Features
Brand
Tascit
Full Details
Dosage Strength
1620mg (Eq. 15mEq)
Drug Ingredients
- Potassium Citrate
Drug Packaging
Extended-Release Tablet 1's
Generic Name
Potassium Citrate
Dosage Form
Extended-Release Tablet
Registration Number
DR-XY44622
Drug Classification
Prescription Drug (RX)
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