Citra-K wax matrix extend-release tablet is indicated in- Renal tubular acidosis (RTA) with calcium stones. Hypocitraturic calcium oxalate nephrolithiasis of any etiology. Uric acid lithiasis with or without calcium stones.
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 urine that is less conducive to the crystallization of stoneforming 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 When the treatment is withdrawn, urinary citrate begins to decline toward the pre-treatment level on the first day.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.
Always consult a registered doctor before taking any medicine. This information is for general knowledge only.
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. Pediatric Use : Safety and effectiveness in children have not been established.
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.
Patients with hyperkalemia (or who have conditions predisposing them to hyperkalemia). Such conditions include chronic renal failure, uncontrolled diabetes mellitus, acute dehydration, strenuous physical exercise in unconditioned individuals, adrenal insufficiency, extensive tissue breakdown. Patients for 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. Patients with peptic ulcer disease. Patients with active urinary tract infection. Patients with renal insufficiency (glomerular filtration rate of less than 0.7 mL/kg/min).
The following drug interactions may occur with Citra-K: Citra-K-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.
Hyperkalemia : In patients with impaired mechanisms for excreting potassium, Citra-K administration can produce hyperkalemia and cardiac arrest. Potentially fatal hyperkalemia can develop rapidly and be asymptomatic. The use of Citra-K 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. Gastrointestinal lesions : if there is severe vomiting, abdominal pain or gastrointestinal bleeding, Citra-K extended-release tablets should be discontinued immediately and the possibility of bowel perforation or obstruction investigated.