DailyMed Label: Potassium Citrate

DailyMed Label: Potassium Citrate

2024

DailyMed Prescription

Potassium Citrate

Potassium Citrate

REMEDYREPACK INC.

NDC: 70518-3160

NDC: 70518-3160

Potassium Citrate Extended-Release Tablets USP are a citrate salt of potassium. Its empirical formula is K 3 C 6 H 5 O 7 • H 2 O, and it has the following chemical structure: Potassium Citrate Extended-Release Tablets USP are off-white to yellow, oral wax-matrix tablets, contain 10 mEq (1080 mg) potassium citrate and 15 mEq (1620 mg) potassium citrate each. Inactive ingredients include carnauba wax and magnesium stearate. Potassium Citrate Extended-Release Tablets USP meet USP Dissolution Test 4 .

Potassium Citrate Extended-Release Tablets are a citrate salt of potassium indicated for the management of: Renal tubular acidosis (RTA) with calcium stones ( 1.1 ) Hypocitraturic calcium oxalate nephrolithiasis of any etiology ( 1.2 ) Uric acid lithiasis with or without calcium stones ( 1.3 )

Objective: To restore normal urinary citrate (greater than 320 mg/day and as close to the normal mean of 640 mg/day as possible), and to increase urinary pH to a level of 6.0 to 7.0. Severe hypocitraturia (urinary citrate < 150 mg/day): therapy should be initiated at 60 mEq per day; a dose of 30 mEq two times per day or 20 mEq three times per day with meals or within 30 minutes after meals or bedtime snack ( 2.2 ) Mild to moderate hypocitraturia (urinary citrate >150 mg/day): therapy should be initiated at 30 mEq per day; a dose of 15 mEq two times per day or 10 mEq three times per day with meals or within 30 minutes after meals or bedtime snack ( 2.3 )

10 mEq extended-release tablets are off-white to yellow in color, capsule shaped, and debossed with “ANI 291”.

Potassium citrate extended-release tablets are contraindicated: In patients with hyperkalemia (or who have conditions pre-disposing 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). 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. In patients with peptic ulcer disease because of its ulcerogenic potential. In patients with active urinary tract infection (with either urea-splitting or other organisms, in association with either calcium or struvite stones). The ability of potassium citrate to increase urinary citrate may be attenuated by bacterial enzymatic degradation of citrate. Moreover, the rise in urinary pH resulting from potassium citrate therapy might promote further bacterial growth. 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.

Hyperkalemia: In patients with impaired mechanisms for excreting potassium, potassium citrate administration can produce hyperkalemia and cardiac arrest. Potentially fatal hyperkalemia can develop rapidly and be asymptomatic. The use of potassium citrate extended-release tablets 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 ( 5.1 ) Gastrointestinal lesions: if there is severe vomiting, abdominal pain or gastrointestinal bleeding, potassium citrate extended-release tablets should be discontinued immediately and the possibility of bowel perforation or obstruction investigated ( 5.2 )

Some patients may develop minor gastrointestinal complaints such as abdominal discomfort, vomiting, diarrhea, loose bowel movements or nausea. These may be alleviated by taking the dose with meals or snacks or by reducing the dosage (

The following drug interactions may occur with potassium citrate: Potassium-sparing diuretics: concomitant administration should be avoided since the simultaneous administration of these agents can produce severe hyperkalemia ( 7.1 ) Drugs that slow gastrointestinal transit time: These agents (such as anticholinergics) can be expected to increase the gastrointestinal irritation produced by potassium salts ( 7.2 ) Renin-angiotensin-aldosterone inhibitors: Monitor for hyperkalemia ( 7.3 ) Nonsteroidal anti-inflammatory drugs (NSAIDs): Monitor for hyperkalemia ( 7.4 )

Pregnant women: Animal reproduction studies have not been conducted. It is not known whether potassium citrate can cause fetal harm when administered to a pregnant woman or can affect reproduction capacity. Potassium citrate extended-release tablets should be given to a pregnant woman only if clearly needed ( 8.1 ) Nursing mothers: The normal potassium ion content of human milk is about 13 mEq/L. It is not known if potassium citrate has an effect on this content. Potassium citrate extended-release tablets should be given to a woman who is breastfeeding only if clearly needed ( 8.3 ) Pediatric Use: Safety and effectiveness in children have not been established ( 8.4 )

Potassium Citrate Extended-Release Tablets USP 10 mEq are off-white to yellow in color, capsule shaped, debossed with “ANI 291” and supplied in NDC: 70518-3160-00 PACKAGING: 100 in 1 BOTTLE PLASTIC Storage: Store at 20° to 25°C (68° to 77°F); excursions permitted at 15° to 30°C (59° to 86°F) [see USP Controlled Room Temperature]. Store in a tight container. Repackaged and Distributed By: Remedy Repack, Inc. 625 Kolter Dr. Suite #4 Indiana, PA 1-724-465-8762

When potassium citrate extended-release tablets are 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 increase 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 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 ion 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 the 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 diarrheal 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.

The pivotal potassium citrate trials were non-randomized and non-placebo controlled where dietary management may have changed coincidentally with pharmacological treatment. Therefore, the results as presented in the following sections may overstate the effectiveness of the product.

DRUG: Potassium Citrate GENERIC: Potassium Citrate DOSAGE: TABLET, EXTENDED RELEASE ADMINSTRATION: ORAL NDC: 70518-3160-0 COLOR: white SHAPE: CAPSULE SCORE: No score SIZE: 18 mm IMPRINT: ANI;291 PACKAGING: 100 in 1 BOTTLE, PLASTIC ACTIVE INGREDIENT(S): POTASSIUM CITRATE 10meq in 1 INACTIVE INGREDIENT(S): MAGNESIUM STEARATE CARNAUBA WAX