Hypophos

N/A

Calcium Acetate is indicated for the control of hyperphosphatemia in end stage renal disease (ESRD) and does not promote aluminum absorption.

N/A

Calcium Acetate is contraindicated in patients with hypercalcemia.

Calcium Acetate when taken with meals, combines with dietary phosphate to form insoluble Calcium Phosphate which is excreted in the feces. Maintenance of serum phosphorus below 6.0 mg/dl is generally considered as a clinically acceptable outcome of treatment with phosphate binders. Calcium Acetate is highly soluble at neutral pH, making the Calcium readily available for binding to phosphate in the proximal small intestine. Orally administered Calcium Acetate from pharmaceutical dosage forms has been demonstrated to be systemically absorbed up to approximately 40% under fasting conditions and up to approximately 30% under non fasting conditions. This range represents data from both healthy subjects and renal dialysis patients under various conditions.

Calcium Acetate may decrease the bioavailability of tetracycline.

Patients may occasionally experience nausea during Calcium Acetate therapy. Hypercalcemia may occur during treatment with Calcium Acetate. Mild hypercalcemia (Ca >10.5 mg/dl) may be asymptomatic or manifest itself as constipation, anorexia, nausea and vomiting. More severe hypercalcemia (Ca >12 mg/dl) is associated with confusion, delirium, stupor and coma. Mild hypercalcemia is easily controlled by reducing the Calcium Acetate dose or temporarily discontinuing therapy. Severe hypercalcemia can be treated by acute hemodialysis and discontinuing Calcium Acetate therapy. Decreasing dialysate calcium concentration could reduce the incidence and severity of Calcium Acetate induced hypercalcemia. The long-term effect of Calcium Acetate on the progression of vascular or soft-tissue calcification has not been determined. Isolated cases of pruritus have been reported which may represent allergic reactions.

Administration of Calcium Acetate in excess of the appropriate daily dosage can cause severe hypercalcemia.

Teratogenic Effects: Category C. Animal reproduction studies have not been conducted with Calcium Acetate. It is also not known whether Calcium Acetate can cause fetal harm when administered to a pregnant woman or can affect reproduction capacity. Calcium Acetate should be given to a pregnant woman only if clearly needed.

Excessive dosage of Calcium Acetate induces hypercalcemia; therefore, early in the treatment during dosage adjustment serum calcium should be determined twice weekly. Should hypercalcemia develop, the dosage should be reduced or the treatment discontinued immediately depending on the severity of hypercalcemia. Calcium Acetate should not be given to patients on digitalis, because hypercalcemia may precipitate cardiac arrhythmias. Calcium Acetate therapy should always be started at low dose and should not be increased without careful monitoring of serum calcium. The patient should be informed about compliance with dosage instructions, adherence to instructions about diet and avoidance of the use of nonprescription antacids. Patients should be informed about the symptoms of hypercalcemia.