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Calcium carbonate hyperphosphatemia

Hyperphosphatemia is generally benign and rarely needs aggressive therapy. Dietary restriction of phosphate and protein is effective for most minor elevations. Phosphate binders such as aluminum-based antacids, calcium carbonate, calcium acetate (PhosLo , Nabi), sevelamer (Renagel , Genzyme), and lanthanum carbonate (Fosrenol , Shire) may be necessary for some patients.43 If patients exhibit findings of hypocalcemia (tetany), IV calcium should be administered empirically. [Pg.415]

Unlabeled Uses Treatment of hyperphosphatemia (calcium carbonate)... [Pg.181]

Because of its potent effects on parathyroid hormone, intestinal calcium absorption, and bone calcium mobilization, calcitriol can cause hypercalcemia, often precluding its use in therapeutic doses (32). Hyperphosphatemia is also a persistent problem in patients on chronic hemodialysis and can be aggravated by therapeutic doses of calcitriol. The use of large doses of calcium carbonate or acetate to control phosphate absorption can increase the risk of hypercalcemia from calcitriol (33). [Pg.3672]

Calcium carbonate is mainly used in oral pharmaceutical formulations and is generally regarded as a nontoxic material. However, calcium carbonate administered orally may cause constipation and flatulence. Consumption of large quantities (4—60g daily) may also result in hypercalcemia or renal impairment. Therapeutically, oral doses of up to about 1.5 g are employed as an antacid. In the treatment of hyperphosphatemia in patients with chronic renal failure, oral daily doses of 2.5-17 g have been used. Calcium carbonate may interfere with the absorption of other drugs from the gastrointestinal tract if administered concomitantly. [Pg.91]

Therapy for hyperphosphatemia is directed toward correcting the cause of the high serum phosphate. In renal failure and in hypoparathyroidism, dietary restriction of phosphate and agents that bind phosphate in the intestine (calcium carbonate and others) are useful in lowering the serum phosphate concentrations. [Pg.1907]

FI 1. Fournier, A., Moriniere, P., Sebert, J. L., et al., Calcium carbonate, an aluminum-free agent for control of hyperphosphatemia, hypocalcemia, and hyperparathyroidism in uremia. Kidney Int. 29, Suppl. 18, 114-119 (1986). [Pg.109]

Patients with end-stage renal disease hyperphosphatemia ineffectively filter excess phosphate that enters the body in the normal diet.278 Elevated phosphate produces the bone disorder renal osteodystrophy. Skeletal deformity may occur, possibly associated with cardiovascular disease. Calcium deposits may further build up around the body and in blood vessels creating further health risks. The use of lanthanum carbonate is being promoted as an alternative to aluminum-based therapies.279,280 Systemic absorption, and cost have produced a clinical candidate, Fosrenol (AnorMED), an intriguing use of a lanthanide compound in therapy. [Pg.834]


See other pages where Calcium carbonate hyperphosphatemia is mentioned: [Pg.466]    [Pg.613]    [Pg.610]    [Pg.886]    [Pg.836]    [Pg.217]    [Pg.175]    [Pg.409]    [Pg.389]    [Pg.887]    [Pg.1935]    [Pg.960]    [Pg.383]    [Pg.159]    [Pg.175]    [Pg.374]   
See also in sourсe #XX -- [ Pg.176 ]




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