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Calcium carbonate is an effective phosphorus binder in children with chronic renal failure
Insights
Calcium carbonate effectively lowers serum phosphorus in children with chronic renal failure. This phosphate binder showed significant reductions in phosphorus levels without altering calcium, bicarbonate, or creatinine.
Area of Science:
- Pediatric Nephrology
- Renal Nutrition
Background:
- Chronic renal failure (CRF) in children often leads to hyperphosphatemia.
- Phosphate binders are crucial for managing mineral and bone disorders in pediatric CRF.
- Aluminum hydroxide, a previous standard, carries risks of aluminum toxicity.
Purpose of the Study:
- To evaluate calcium carbonate as a safe and effective phosphate binder in pediatric CRF.
- To compare its efficacy with prior aluminum hydroxide treatment.
Main Methods:
- A study involving 19 children with CRF, some on dialysis (CAPD/hemodialysis).
- Assessed serum phosphorus, calcium, bicarbonate, and creatinine levels before and during calcium carbonate therapy.
- Monitored serum aluminum levels in children previously treated with aluminum hydroxide.
Main Results:
- Calcium carbonate significantly reduced serum phosphorus from 7.4 to 5.9 mg/dL (P < .001) without affecting other key parameters.
- Serum aluminum levels decreased significantly after discontinuing aluminum hydroxide.
- Parathyroid hormone (PTH) levels decreased in children initially treated with calcium carbonate.
Conclusions:
- Calcium carbonate is an effective phosphate binder for children with chronic renal failure.
- It offers a safer alternative to aluminum hydroxide, with manageable side effects like hypercalcemia.
- Further research may explore optimal dosing and long-term outcomes.
Abstract:
We evaluated the effectiveness of calcium carbonate as a phosphate binder in 19 children with chronic renal failure; ten children were undergoing dialysis therapy (eight maintained by CAPD and two by hemodialysis). Twelve children had previously received aluminum hydroxide, while calcium carbonate was the primary phosphate binder used in seven children. Among all the children, the serum phosphorus level on no phosphate binder was 7.4 +/- 0.9 mg/dL, which decreased significantly (P less than .001) to 5.9 +/- 0.8 mg/dL during calcium carbonate therapy, while the serum calcium, bicarbonate, and creatinine were unchanged. The reduction in the serum phosphorus level occurred while dietary intake of calcium and phosphorus were unchanged, as demonstrated by three-day dietary records. The dose of calcium carbonate required to maintain the serum phosphorus in the normal range varied from 600 mg to 15 g/d (mean 7.4 g/d). Among the 12 children and four others who had received aluminum hydroxide, serum aluminum levels fell from 108.8 +/- 121.8 ng/mL to 36.1 +/- 29.1 ng/mL after aluminum hydroxide was stopped (P less than .05). Serum alkaline phosphatase and parathyroid hormone (PTH) levels during aluminum hydroxide therapy were similar to levels obtained during calcium carbonate therapy, while PTH levels fell in children treated initially with calcium carbonate. All the children have been observed for a mean of 12.0 months (range 4 months to 3 1/2 years). Hypercalcemia occurred in seven children, usually when vitamin D therapy was initiated or the dose changed. Hypercalcemia resolved with adjustment of the vitamin D or calcium carbonate dose in all but one patient.(ABSTRACT TRUNCATED AT 250 WORDS)