Berkley and Jensen Acid Controller Complete and Renal dysfunction

Absorption of oral calcium formulations may be altered and elimination of calcium by the kidney decreased with renal impairment. Hyperphosphatemia occurs during renal failure. Calcium acetate or calcium carbonate, in addition to providing calcium, complexes phosphates within the GI tract. Calcium carbonate can partially correct metabolic acidosis associated with chronic renal failure. Clinical monitoring of renal function and serum calcium and phosphate concentrations is necessary.

Magnesium is eliminated by the kidney. The serum concentration of magnesium is increased in patients with renal impairment. Magnesium toxicity includes CNS depression, muscular paralysis, respiratory depression, hypotension and prolonged cardiac conduction time. Disappearance of the patellar reflex is a useful clinical sign of magnesium intoxication. Therapy with magnesium should be administered cautiously and dosages should be modified in patients with compromised renal function. Clinical monitoring of serum magnesium levels is recommended.

Famotidine is partially eliminated by the kidney as unchanged drug, the extent of which is dependent upon the route of administration (25% to 30% oral; 65% to 70% intravenous). The elimination half-life of famotidine may be prolonged considerably in patients with severe renal impairment (CrCl < 10 mL/min), possibly exceeding 20 hours and approaching approximately 24 hours in anuric patients. Since central nervous system adverse effects such as grand mal seizures and psychic disturbances have been reported in patients with moderate (CrCl < 50 mL/min) and severe renal impairment, dosage adjustments are recommended for these patients. Reducing the normally recommended dosage by one-half or prolonging the dosing interval to 36 to 48 hours may be appropriate, depending on the patient's clinical response.