Urocit-K (potassium citrate) Drug Facts and Product Info

About Urocit^®-K

Urocit^®-K is a citrate salt of potassium. Its empirical formula is K₃C₆H₅0₇ · H₂0.

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.

Dosage forms and strengths

5 mEq tablets are uncoated, tan to yellowish in color, modified ball shaped, with MPC 600 debossed on one side and blank on the other
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

Clinical pharmacology

Mechanism of action

When Urocit^®-K 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, Urocit^®-K 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, Urocit^®-K increases urinary potassium by approximately the amount contained in the medication. In some patients, Urocit^®-K causes a transient reduction in urinary calcium.

The changes induced by Urocit^®-K 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.

Urocit^®-K 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 Urocit^®-K dosage. Following long-term treatment, Urocit^®-K 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), Urocit^®-K may be relatively ineffective in raising urinary citrate. A higher dose of Urocit^®-K may therefore be required to produce a satisfactory citraturic response. In patients with renal tubular acidosis in whom urinary pH may be high, Urocit^®-K produces a relatively small rise in urinary pH.

Important Safety Information

Contraindications

Patients with hyperkalemia, peptic ulcer disease, active urinary tract infection, and renal insufficiency
Conditions predisposing patients to hyperkalemia, including chronic renal failure, uncontrolled diabetes mellitus, acute dehydration, strenuous physical exercise in unconditioned individuals, adrenal insufficiency, and extensive tissue breakdown

Warnings and Precautions

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

Patient Counseling Information

Administration of Drug

Patients should be told to take Urocit-K 15 mEq without crushing, chewing, or sucking the tablet
Patients should be told to take Urocit-K 15 mEq only as directed, especially if the patient is also taking both diuretics and digitalis preparations
Patients should be told to check with the doctor if they experience difficulty swallowing the tablet or it seems to stick in the throat
Patients should be told to check with the doctor at once if they notice tarry stools or other signs of gastrointestinal bleeding
Patients should be advised that regular blood tests and electrocardiograms will be performed to ensure safety

Patient Monitoring Information

Hyperkalemia

Patients with impaired mechanisms for excreting potassium should be closely monitored for signs of hyperkalemia with periodic blood tests and ECGs

This material is intended to provide basic information. Patients should discuss all medical advice, diagnosis, and treatment with their healthcare provider.

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