Urocit-K is a citrate salt of potassium. Its empirical formula is K3C6H507 • H20, and it has the following chemical structure: Urocit-K yellowish to tan, oral wax-matrix tablets, contain 5 mEq (540 mg) potassium citrate, 10 mEq (1080 mg) potassium citrate and 15 mEq (1620 mg) potassium citrate each. Inactive ingredients include carnauba wax and magnesium stearate. Structure

1.1 Renal Tubular Acidosis (RTA) with Calcium Stones Potassium citrate is indicated for the management of renal tubular acidosis

Hypocitraturic Calcium Oxalate Nephrolithiasis of any Etiology Potassium citrate is indicated for the management of Hypocitraturic calcium oxalate nephrolithiasis

Uric Acid Lithiasis with or without Calcium Stones Potassium citrate is indicated for the management of Uric acid lithiasis with or without calcium stones . Urocit-K is a citrate salt of potassium indicated 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

10 mEq tablets are uncoated, tan to yellowish in color, elliptical shaped, with 610 debossed on one side and MISSION on the other 15 mEq tablets are uncoated, tan to yellowish in color, modified rectangle shaped, with M15 debossed on one side and blank on the other Tablets: 10 mEq and 15 mEq

2.1 Dosing Instructions Treatment with extended release potassium citrate should be added to a regimen that limits salt intake (avoidance of foods with high salt content and of added salt at the table) and encourages high fluid intake (urine volume should be at least two liters per day). The objective of treatment with Urocit-K is to provide Urocit-K in sufficient dosage 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 or 7.0. Monitor serum electrolytes (sodium, potassium, chloride and carbon dioxide), serum creatinine and complete blood counts every four months and more frequently in patients with cardiac disease, renal disease or acidosis. Perform electrocardiograms periodically. Treatment should be discontinued if there is hyperkalemia, a significant rise in serum creatinine or a significant fall in blood hematocrit or hemoglobin

Severe Hypocitraturia In patients with severe hypocitraturia (urinary citrate < 150 mg/day), therapy should be initiated at a dosage of 60 mEq/day (30 mEq two times/day or 20 mEq three times/day with meals or within 30 minutes after meals or bedtime snack). 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. Doses of Urocit-K greater than 100 mEq/day have not been studied and should be avoided

Mild to Moderate Hypocitraturia In patients with mild to moderate hypocitraturia (urinary citrate > 150 mg/day) therapy should be initiated at 30 mEq/day (15 mEq two times/day or 10 mEq three times/day with meals or within 30 minutes after meals or bedtime snack). 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. Doses of Urocit-K greater than 100 mEq/day have not been studied and should be avoided. 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 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

5.1 Hyperkalemia In patients with impaired mechanisms for excreting potassium, Urocit-K administration can produce hyperkalemia and cardiac arrest. Potentially fatal hyperkalemia can develop rapidly and be asymptomatic. The use of Urocit-K 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. Closely monitor for signs of hyperkalemia with periodic blood tests and ECGs

Gastrointestinal Lesions Solid dosage forms of potassium chlorides have produced stenotic and/or ulcerative lesions of the small bowel and deaths. These lesions are caused by a high local concentration of potassium ions in the region of the dissolving tablets, which injured the bowel. In addition, perhaps because wax-matrix preparations are not enteric-coated and release some of their potassium content in the stomach, there have been reports of upper gastrointestinal bleeding associated with these products. The frequency of gastrointestinal lesions with wax-matrix potassium chloride products is estimated at one per 100,000 patient-years. Experience with Urocit-K is limited, but a similar frequency of gastrointestinal lesions should be anticipated. If there is severe vomiting, abdominal pain or gastrointestinal bleeding, Urocit-K should be discontinued immediately and the possibility of bowel perforation or obstruction investigated. Hyperkalemia: In patients with impaired mechanisms for excreting potassium, Urocit-K administration can produce hyperkalemia and cardiac arrest. Potentially fatal hyperkalemia can develop rapidly and be asymptomatic. The use of Urocit-K 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 Gastrointestinal lesions: if there is severe vomiting, abdominal pain or gastrointestinal bleeding, Urocit-K should be discontinued immediately and the possibility of bowel perforation or obstruction investigated

7.1 Potential Effects of Potassium Citrate on Other Drugs Potassium-sparing Diuretics: Concomitant administration of Urocit-K 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

Potential Effects of Other Drugs on Potassium Citrate Drugs that slow gastrointestinal transit time: These agents (such as anticholinergics) can be expected to increase the gastrointestinal irritation produced by potassium salts

Renin-Angiotensin-Aldosterone System Inhibitors Drugs that inhibit the renin-angiotensin-aldosterone system (RAAS) including angiotensin converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARBs), spironolactone, eplerenone, or aliskiren produce potassium retention by inhibiting aldosterone production. Closely monitor potassium in patients receiving concomitant RAAS therapy

Nonsteroidal Anti-Inflammatory Drugs (NSAIDs) NSAIDs may produce potassium retention by reducing renal synthesis of prostagladin E and impairing the renin-angiotensin system. Closely monitor potassium in patients on concomitant NSAIDs. 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 Drugs that slow gastrointestinal transit time: These agents (such as anticholinergics) can be expected to increase the gastrointestinal irritation produced by potassium salts Renin-angiotensin-aldosterone inhibitors: Monitor for hyperkalemia Nonsteroidal Anti-inflammatory drugs (NSAIDs) monitor for hyperkalemia