K-XR Potassium Citrate 1080mg Extended-Release Tablet 30's
RXDRUG-DRP-4840-05
Discreet Packaging
FDA-registered Products
FDA-licensed Pharmacies
Indications/Uses
Potassium citrate is indicated for the management of renal tubular acidosis (RTA) with calcium stones, hypocitraturic calcium oxalate nephrolithiasis of any etiology, and uric acid lithiasis with or without calcium stones.
Dosage/Direction for Use
In patients with severe hypocitraturia (urinary citrate of less than 150 mg/day), therapy should be initiated at a dosage of 60 meq/day (20 meq three times/day or 15 meq four times/day with meals or within 30 minutes after meals or bedtime snack). In patients with mild-moderate hypocitraturia (>150 mg/day), Potassium Citrate Tablet should be initiated at a dosage of 30 meq/day (10 meq three times/day with meals). Twenty-four hour urinary citrate and/or urinary pH measurements should be used to determine the adequacy of the initial dosage and to evaluate the effectiveness of any dosage change. In addition, urinary citrate and/or pH should be measured every four months.
Administration
Should be taken with food: Take w/ meals or w/in 30 min after meals or bedtime snack.
Contraindications
Potassium Citrate tablet is contraindicated in patients with hyperkalemia (or who have conditions predisposing them to hyperkalemia), as a further rise in serum potassium concentration may produce cardiac arrest. Such conditions include: chronic renal failure, uncontrolled diabetes mellitus, acute dehydration, strenuous physical exercise in unconditioned individuals, adrenal insufficiency, extensive tissue breakdown, or the administration of a potassium-sparing agent (such as triamterene, spironolactone or amiloride).
Potassium Citrate Tablet is contraindicated in patients in whom there is cause for arrest or delay in tablet passage through the gastrointestinal tract, such as those suffering from delayed gastric emptying, esophageal compression, intestinal obstruction or stricture or those taking anticholinergic medication. Because of its ulcerogenic potential, Potassium Citrate Tablet should not be given to patients with peptic ulcer disease. Potassium Citrate Tablet is contraindicated in patients with renal insufficiency (glomerular filtration rate of less than 0.7 mL/kg/min), because of the danger of soft tissue calcification and increased risk for the development of hyperkalemia. Or as prescribed by the physician.
Potassium Citrate Tablet is contraindicated in patients in whom there is cause for arrest or delay in tablet passage through the gastrointestinal tract, such as those suffering from delayed gastric emptying, esophageal compression, intestinal obstruction or stricture or those taking anticholinergic medication. Because of its ulcerogenic potential, Potassium Citrate Tablet should not be given to patients with peptic ulcer disease. Potassium Citrate Tablet is contraindicated in patients with renal insufficiency (glomerular filtration rate of less than 0.7 mL/kg/min), because of the danger of soft tissue calcification and increased risk for the development of hyperkalemia. Or as prescribed by the physician.
Special Precautions
Hyperkalemia: in patients with impaired mechanisms for excreting potassium, Potassium Citrate Tablet administration can produce hyperkalemia and cardiac arrest. Potentially fatal hyperkalemia can develop rapidly and be asymptomatic. The use of Potassium Citrate Tablet in patients with chronic renal failure, or any other condition which impairs potassium excretion such as severe myocardial damage or heart failure, should be avoided.
Interaction with potassium-sparing diuretics: concomitant administration of Potassium Citrate Tablet and a potassium-sparing diuretic (such as triamterene, spironolactone or amiloride) should be avoided, since the simultaneous administration of these agents can produce severe hyperkalemia. If there is severe vomiting, abdominal pain or gastrointestinal bleeding, Potassium Citrate Tablet should be discontinued immediately and the possibility of bowel perforation or obstruction investigated.
Precautions: Physicians should consider reminding the patient of the following: To take each dose without crushing, chewing or sucking the tablet, to take this medicine only as directed. This is especially important if the patient is also taking both diuretics and digitalis preparations, to check with physician if there is trouble swallowing tablets or if the tablet seems to stick in the throat, to check with the doctor at once if tarry stools or other evidence of gastrointestinal bleeding is noticed.
Interaction with potassium-sparing diuretics: concomitant administration of Potassium Citrate Tablet and a potassium-sparing diuretic (such as triamterene, spironolactone or amiloride) should be avoided, since the simultaneous administration of these agents can produce severe hyperkalemia. If there is severe vomiting, abdominal pain or gastrointestinal bleeding, Potassium Citrate Tablet should be discontinued immediately and the possibility of bowel perforation or obstruction investigated.
Precautions: Physicians should consider reminding the patient of the following: To take each dose without crushing, chewing or sucking the tablet, to take this medicine only as directed. This is especially important if the patient is also taking both diuretics and digitalis preparations, to check with physician if there is trouble swallowing tablets or if the tablet seems to stick in the throat, to check with the doctor at once if tarry stools or other evidence of gastrointestinal bleeding is noticed.
Adverse Reactions
Some patients may develop minor gastrointestinal complaints during potassium citrate therapy, such as abdominal discomfort, vomiting, diarrhea, loose bowel movements or nausea. These symptoms are due to the irritation of the gastrointestinal tract, and may be alleviated by taking the dose with meals or snack, or by reducing the dosage. Patients may find intact matrices in feces.
Drug Interactions
Concomitant administration of potassium citrate and a potassium-sparing diuretic (such as triamterene, spironolactone or amiloride) should be avoided, since the simultaneous administration of these agents can produce severe hyperkalemia.
Storage
Store at temperatures not exceeding 30°C.
Action
Pharmacology: Pharmacodynamics: Mechanism of Action: Potassium citrate, which works by restoring naturally occurring chemicals in the urine that stop crystals from forming and also inhibits the formation of the 2 most common types of kidney stones, calcium oxalate and uric acid stones. In numerous studies, patients treated with Potassium Citrate have demonstrated significantly lower rates of kidney stone formation. In many patients, new stones do not form at all.
Pharmacokinetics: When potassium citrate is given orally, the metabolism of absorbed citrate produces an alkaline load. The induced alkaline load in turn increases urinary pH and raises urinary citrate by augmenting citrate clearance without measurably altering ultrafilterable serum citrate. Thus, potassium citrate therapy appears to increase urinary citrate principally by modifying the renal handling of citrate, rather than by increasing the filtered load of citrate. The increased filtered load of citrate may play some role, however, as in small comparisons of oral citrate and oral bicarbonate, citrate had a greater effect on urinary citrate.
In addition to raising urinary pH and citrate, potassium citrate increases urinary potassium by approximately the amount contained in the medication. In some patients, potassium citrate causes a transient reduction in urinary calcium.
The changes induced by potassium citrate produce a urine that is less conducive to the crystallization of stone-forming salts (calcium oxalate, calcium phosphate and uric acid). Increased citrate in the urine, by complexing with calcium, decreases calcium on activity and thus the saturation of calcium oxalate. Citrate also inhibits the spontaneous nucleation of calcium oxalate and calcium phosphate (brushite).
The increase in urinary pH also decreases calcium ion activity by increasing calcium complexation to dissociated anions. The rise in urinary pH also increases the ionization of uric acid to more soluble urate ion.
Potassium citrate therapy does not alter the urinary saturation of calcium phosphate, since the effect of increased citrate complexation of calcium is opposed by the rise in pH-dependent dissociation of phosphate. Calcium phosphate stones are more stable in alkaline urine.
In the setting of normal renal function, the rise in urinary citrate following a single dose begins by the first hour and lasts for 12 hours.
With multiple doses the rise in citrate excretion reaches its peak by the third day and averts the normally wide circadian fluctuation in urinary citrate, thus maintaining urinary citrate at a higher, more constant level throughout the day. When the treatment is withdrawn, urinary citrate begins to decline toward the pre-treatment level on the first day.
The rise in citrate excretion is directly dependent on the potassium citrate dosage. Following long-term treatment, potassium citrate at a dosage of 60 mEq/day raises urinary citrate by approximately 400 mg/day and increases urinary pH by approximately 0.7 units.
In patients with severe renal tubular acidosis or chronic diarrhea syndrome where urinary citrate may be very low (<100 mg/day), potassium citrate may be relatively ineffective in raising urinary citrate. A higher dose of potassium citrate may therefore be required to produce a satisfactory citraturic response. In patients with renal tubular acidosis in whom urinary pH may be high, potassium citrate produces a relatively small rise in urinary pH.
Pharmacokinetics: When potassium citrate is given orally, the metabolism of absorbed citrate produces an alkaline load. The induced alkaline load in turn increases urinary pH and raises urinary citrate by augmenting citrate clearance without measurably altering ultrafilterable serum citrate. Thus, potassium citrate therapy appears to increase urinary citrate principally by modifying the renal handling of citrate, rather than by increasing the filtered load of citrate. The increased filtered load of citrate may play some role, however, as in small comparisons of oral citrate and oral bicarbonate, citrate had a greater effect on urinary citrate.
In addition to raising urinary pH and citrate, potassium citrate increases urinary potassium by approximately the amount contained in the medication. In some patients, potassium citrate causes a transient reduction in urinary calcium.
The changes induced by potassium citrate produce a urine that is less conducive to the crystallization of stone-forming salts (calcium oxalate, calcium phosphate and uric acid). Increased citrate in the urine, by complexing with calcium, decreases calcium on activity and thus the saturation of calcium oxalate. Citrate also inhibits the spontaneous nucleation of calcium oxalate and calcium phosphate (brushite).
The increase in urinary pH also decreases calcium ion activity by increasing calcium complexation to dissociated anions. The rise in urinary pH also increases the ionization of uric acid to more soluble urate ion.
Potassium citrate therapy does not alter the urinary saturation of calcium phosphate, since the effect of increased citrate complexation of calcium is opposed by the rise in pH-dependent dissociation of phosphate. Calcium phosphate stones are more stable in alkaline urine.
In the setting of normal renal function, the rise in urinary citrate following a single dose begins by the first hour and lasts for 12 hours.
With multiple doses the rise in citrate excretion reaches its peak by the third day and averts the normally wide circadian fluctuation in urinary citrate, thus maintaining urinary citrate at a higher, more constant level throughout the day. When the treatment is withdrawn, urinary citrate begins to decline toward the pre-treatment level on the first day.
The rise in citrate excretion is directly dependent on the potassium citrate dosage. Following long-term treatment, potassium citrate at a dosage of 60 mEq/day raises urinary citrate by approximately 400 mg/day and increases urinary pH by approximately 0.7 units.
In patients with severe renal tubular acidosis or chronic diarrhea syndrome where urinary citrate may be very low (<100 mg/day), potassium citrate may be relatively ineffective in raising urinary citrate. A higher dose of potassium citrate may therefore be required to produce a satisfactory citraturic response. In patients with renal tubular acidosis in whom urinary pH may be high, potassium citrate produces a relatively small rise in urinary pH.
MedsGo Class
Other Drugs Acting on the Genito-Urinary System
Features
Brand
K-Xr
Full Details
Dosage Strength
1080 mg
Drug Ingredients
- Potassium Citrate
Drug Packaging
Extended-Release Tablet 30's
Generic Name
Potassium Citrate
Dosage Form
Extended-Release Tablet
Registration Number
DRP-4840-05
Drug Classification
Prescription Drug (RX)
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