Calcium Carbonate as a Phosphate Binder in Patients with Chronic Renal Failure Undergoing Dialysis

• Published in: The New England journal of medicine Vol. 315; no. 3; pp. 157 - 161
• Main Authors: Slatopolsky, Eduardo, Weerts, Carol, Lopez-Hilker, Silvia, Norwood, Kathryn, Zink, Mary, Windus, David, Delmez, James
• Format: Journal Article
• Language: English
• Published: Boston, MA Massachusetts Medical Society 17.07.1986
• Subjects: Adult; Aged; Aluminum; Aluminum hydroxide; Aluminum Hydroxide - adverse effects; Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy; Biological and medical sciences; Bone diseases; Calcification; Calcium - blood; Calcium carbonate; Calcium Carbonate - therapeutic use; Calcium phosphates; Dialysis; Dietitians; Emergency and intensive care: renal failure. Dialysis management; Enzymes; Female; Hemodialysis; Humans; Hyperparathyroidism - prevention & control; Hyperphosphatemia; Intensive care medicine; Kidney Failure, Chronic - blood; Kidney Failure, Chronic - complications; Kidneys; Male; Medical sciences; Medicine; Metastases; Middle Aged; Osteomalacia; Osteomalacia - prevention & control; Patients; Phosphate; Phosphates - blood; Phosphorus; Renal Dialysis; Renal failure; Human; Phosphates; Extrarenal dialysis; Maintenance hemodialysis; Calcium Carbonates; Metabolism; Resuscitation
• ISSN: 0028-4793; 1533-4406
• DOI: 10.1056/NEJM198607173150304

Phosphate binders that contain aluminum are frequently prescribed to treat hyperphosphatemia in patients with chronic renal failure, but an accumulation of aluminum can lead to osteomalacia. To evaluate the efficacy of calcium carbonate as an alternative phosphate binder, we studied 20 patients maintained on dialysis during three consecutive periods. In period 1, the patients took aluminum hydroxide for a month (mean dose, 5.6 g per day; range, 1.5 to 14.0). In period 2, they took no phosphate binders for a month, and in period 3, they took calcium carbonate (Os-Cal) for two months (mean dose, 8.5 g per day; range, 2.5 to 17). The mean (±SE) serum calcium level during period 1 was 9.6±0.2 mg per deciliter; this decreased slightly (to 9.3±0.1) during period 2 and increased to 10.0±0.2 during period 3. The mean (±SE) serum phosphorus level during period 1 was 4.8±0.1 mg per deciliter; this increased to 7.3±0.3 during period 2, but returned to the control value (4.8±0.2) during period 3. Six of the 20 patients continued to need aluminum hydroxide during period 3 for satisfactory control of hyperphosphatemia. Calcium carbonate successfully lowered serum phosphorus levels and raised serum calcium levels in the majority of our patients, thereby confirming that this agent may be a satisfactory substitute for traditional phosphate binders that contain aluminum. The possibility that long-term treatment could cause such side effects as metastatic calcification will require further investigation. (N Engl J Med 1986;315:157–61.) Hyperphosphatemia has a key role in the development of secondary hyperparathyroidism and renal osteodystrophy in patients with uremia. Although controversy exists 1 regarding the exact mechanism by which retention of phosphate produces secondary hyperparathyroidism, it is clear that if hyperphosphatemia can be avoided, secondary hyperparathyroidism can be prevented. 2 3 4 5 Although serum phosphorus does not itself directly affect the acute release of parathyroid hormone, it plays an important part in the regulation of parathyroid hormone secretion by inducing reciprocal changes in the serum concentrations of ionized calcium and 1α,25-dihydroxyvitamin D 3 (1,25(OH) 2 D 3 ). 6 It has been known for many years . . .