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Safety and efficacy of calcium carbonate in children with chronic renal failure
Insights
Calcium carbonate is safe for children with chronic renal failure, despite hypercalcemia risks. Close monitoring is key, and benefits outweigh risks compared to aluminum binders.
Area of Science:
- Pediatric Nephrology
- Clinical Pharmacology
Background:
- Chronic renal failure (CRF) in children necessitates management of mineral and bone disorders.
- Aluminum-based phosphate binders pose risks, prompting investigation of alternatives like calcium carbonate.
Purpose of the Study:
- To assess the safety and efficacy of calcium carbonate in pediatric patients with chronic renal failure.
- To evaluate the incidence and risk factors for hypercalcemia during calcium carbonate therapy.
Main Methods:
- A cohort of 68 children with CRF received calcium carbonate therapy.
- Data collected included serum calcium, GFR, aluminum levels, and incidence of hypercalcemia and nephrocalcinosis.
- Follow-up averaged 19.9 months.
Main Results:
- Hypercalcemia occurred in 29 children (47 episodes), with higher incidence in those with GFR < 15 ml/min/1.73 m2 and on dialysis.
- Calcium carbonate effectively controlled secondary hyperparathyroidism and reduced serum aluminum.
- Nephrocalcinosis was observed in 2 of 23 hypercalcemic patients; no other ectopic calcification was detected.
Conclusions:
- Calcium carbonate is a safe and effective treatment for pediatric chronic renal failure, offering benefits over aluminum binders.
- Close biochemical monitoring is essential to manage hypercalcemia risk, especially in patients with severely reduced GFR.
- Reduced renal homeostatic reserve is a key factor predisposing to hypercalcemia in this population.
Abstract:
The safety and clinical efficacy of calcium carbonate therapy in children with chronic renal failure were assessed in 68 patients (average age 8.38 years) during a mean follow-up period of 19.9 months (range 1.2-49.4). Forty-seven episodes of hypercalcaemia occurred in 29 children (3.5 episodes per 100 patient-months). There were no significant differences in mean GFR or biochemical parameters between these patients at the start of calcium carbonate therapy and the group of children who never experienced hypercalcaemia. Good control of secondary hyperparathyroidism and a significant reduction in serum aluminum were achieved. Two of 23 hypercalcaemic patients showed nephrocalcinosis on ultrasonography. 99Tc pyrophosphate scanning failed to detect any other ectopic calcification. The incidence of hypercalcaemia increased significantly when the GFR was less than 15 ml/min per 1.73 m2 and was most frequent in children receiving dialysis (48 episodes per 100 patient-months). The decrease in GFR during therapy was significantly more in the hypercalcaemic group compared to the normocalcaemic group (P less than 0.01), despite no irreversible acute effects of hypercalcaemia being observed on the rate of decline of GFR. We believe that the reduced renal homeostatic reserve is a major factor predisposing to hypercalcaemia. Consequently calcium carbonate is safe to use in children with severe chronic renal failure with close biochemical monitoring; the benefits over aluminium phosphate binders far outweigh the risks of hypercalcaemia and ectopic calcification.