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Query: UMLS:C0020437 (hypercalcemia)
 10,293 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Calcium carbonate has been successfully used as a phosphate binder in patients with chronic renal failure; however, a high frequency of hypercalcaemia has been reported. To study the effects of calcium carbonate preparations with different dissolution characteristics on the incidence of this side effect, we conducted a double-blind, crossover trial in 21 patients undergoing chronic haemodialysis. Aluminum hydroxide therapy was replaced with calcium carbonate. The subjects then randomly received either an enteric-coated or a gastric-coated preparation. Calcium carbonate (3.1-3.6 g/d) controlled serum phosphate concentrations as effectively as aluminium hydroxide (2.9 g/d). Concurrently, there was a significant rise in mean serum calcium and a fall in serum concentrations of both parathyroid hormone and osteocalcin, the latter suggesting a decrease in bone turnover. Overall, hypercalcaemic episodes developed in 9 patients (43%) and occurred at a considerable frequency (33 episodes per 100 patient-months) during treatment with the gastric-coated formulation. Following conversion to enteric-coated calcium carbonate (3.6 g/d) patients had fewer occurrences of hypercalcaemia (12 episodes per 100 patient-months, P less than 0.05) and, as compared to the gastric-coated preparation, increases in serum calcium greater than 3.00 mmol/l were not observed at all. Hyperaluminaemia was regressive during therapy with calcium carbonate, but addition of small doses of aluminium hydroxide caused a large rise in serum aluminium concentrations after infusion of desferrioxamine, indicating an enhanced rate of absorption or aberrant compartmentalization of aluminium. We conclude that calcium carbonate can control hyperphosphataemia in dialysis patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Calcium carbonate as a phosphate binder in dialysis patients: evaluation of an enteric-coated preparation and effect of additional aluminium hydroxide on hyperaluminaemia. 202 71

Calcium acetate is a potent phosphate binder that causes fewer problems with hypercalcemia and elevated serum aluminum concentrations than other calcium salt or aluminum-binding agents. It exceeds calcium carbonate in its binding ability and is not expensive. These advantages make it an attractive alternative to many of the standard phosphate-binding regimens.
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PMID:Medication review: an alternative phosphate binder--calcium acetate. 206 59

Eight children with terminal renal insufficiency on continuous ambulatory peritoneal dialysis were followed for 12 months to evaluate laboratory parameters of mineral ion and bone metabolism. Calcium carbonate (range 47-295 mg/kg body weight per day) was given in combination with low doses of either vitamin D or 1,25(OH2D3. Blood urea nitrogen and serum phosphate concentrations remained well controlled throughout the observation period. A significant increase in serum calcium levels from 2.35 +/- 0.18 to 2.61 +/- 0.22 mmol/l (mean +/- SD) was observed during the first 6 months. Alkaline phosphatase activity and mid-C-regional parathyroid hormone, both indirect parameters of bone metabolism, revealed no evidence of severe secondary hyperparathyroidism. Our data indicate that calcium carbonate may be sufficient to induce relative hypercalcaemia in uraemic children, and thus reduce the risk of developing renal osteodystrophy. Unwanted side-effects of vitamin D preparations, i.e. increased intestinal phosphate absorption and hypercalcaemia after successful renal transplantation, may thus be avoided.
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PMID:Efficacy of calcium carbonate and low-dose vitamin D/1,25(OH)2D3 in reducing the risk of developing renal osteodystrophy in children on continuous ambulatory peritoneal dialysis. 208 63

Fourteen of 39 dialysis patients (36%) became hypercalcemic after switching to calcium carbonate as their principal phosphate binder. In order to identify risk factors associated with the development of hypercalcemia, indirect parameters of intestinal calcium reabsorption and bone turnover rate in these 14 patients were compared with results in 14 eucalcemic patients matched for age, sex, length of time on dialysis, and etiology of renal disease. In addition to experiencing hypercalcemic episodes with peak calcium values of 2.7 to 3.8 mmol/L (10.7 to 15.0 mg/dL), patients in the hypercalcemic group exhibited a significant increase in the mean calcium concentration obtained during 6 months before the switch, compared with the mean value obtained during the 7 months of observation after the switch (2.4 +/- 0.03 to 2.5 +/- 0.03 mmol/L [9.7 +/- 0.2 to 10.2 +/- 0.1 mg/dL], P = 0.006). In contrast, eucalcemic patients exhibited no change in mean calcium values over the same time period (2.3 +/- 0.05 to 2.3 +/- 0.05 mmol/L [9.2 +/- 0.2 to 9.2 +/- 0.2 mg/dL]). CaCO3 dosage, calculated dietary calcium intake, and circulating levels of vitamin D metabolites were similar in both groups. Physical activity index and predialysis serum bicarbonate levels also were similar in both groups. However, there was a significant difference in parameters reflecting bone turnover rates between groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Etiology of hypercalcemia in hemodialysis patients on calcium carbonate therapy. 223 37

The widespread use of calcium carbonate as a phosphate binder is limited by its tendency to develop hypercalcemia in some patients using effective dosages needed to control hyperphosphatemia. Most common continuous ambulatory peritoneal dialysis (CAPD) regimens using dialysis solutions containing 3.5 mEq/L of calcium result in net absorption of calcium from the dialysis solution and, hence limit the amount of oral calcium that can be administered. Peritoneal dialysis solutions with reduced calcium levels are needed for effective use of CaCO3 to control hyperphosphatemia in some dialysis patients.
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PMID:Calcium carbonate as a phosphate binder: is there a need to adjust peritoneal dialysate calcium concentrations for patients using CaCO3? 248 89

To reduce potentially toxic aluminium exposure, the phosphate binding agent aluminium hydroxide was replaced by high-dose oral calcium carbonate in 15 haemodialysis patients. Stepwise reduction in dialysate calcium concentration (from 1.75 to 1.35 mmol/l and then to 1.05 mmol/l) was made when necessitated by hypercalcaemia. After 6 months, the mean daily dose of calcium carbonate was 62 mmol (range 25-150 mmol). This dose maintained good control of plasma phosphate (baseline, 1.34 +/- 0.32 mmol/l (mean +/- SD); 12 weeks, 1.30 +/- 0.22 mmol/l; 24 weeks, 1.51 +/- 0.31 mmol/l). Calcium x phosphate product did not rise significantly (baseline, 3.41; 12 weeks, 3.44; 24 weeks, 4.02). Apart from a transient early increase, ionised calcium did not change significantly (baseline, 1.23 +/- 0.10 mmol/l; 12 weeks, 1.24 +/- 0.10 mmol/l). Intact (1-84) parathyroid hormone concentration decreased from 241 pg/ml to 116 pg/ml (median values, P less than 0.05) after 12 weeks. This simple and well-tolerated regimen almost completely eliminated oral aluminium exposure, effectively controlled plasma phosphate and calcium concentrations, and reduced hyperparathyroidism.
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PMID:High-dose calcium carbonate with stepwise reduction in dialysate calcium concentration: effective phosphate control and aluminium avoidance in haemodialysis patients. 251 88

Substitution of calcium carbonate for aluminum hydroxide in patients on dialysis: effects on acidosis, parathyroid function, and calcemia. We studied the effects of substituting CaCO3 for aluminum-containing gels on metabolic acidosis and on the response of the parathyroid glands in 11 patients treated with chronic hemodialysis. The 8 men and 3 women were clinically stable, were known to be compliant, and had no clinical evidence of aluminum overload; they were not receiving vitamin D supplements; and they had been on dialysis for an average of 65.6 months (range: 13-188 months). After 3 weeks of CaCO3 administration plasma phosphate concentration remained well controlled, and plasma calcium concentration increased from 9.2 +/- 0.2 (2.3 +/- 0.1 mmol/l) to 10.1 +/- 0.2 mg/dl (2.5 +/- 0.1 mmol/l). Predialysis plasma bicarbonate concentration increased from 19.7 +/- 0.6 to 21.9 +/- 0.6 mmol/l. Plasma aluminum concentration decreased from 78.7 +/- 12.5 to 48.5 +/- 3.9 micrograms/l. Plasma PTH level increased from 2.0 +/- 0.7 to 3.3 +/- 0.8 ng/ml despite the concurrent increase in plasma calcium levels. All values returned to control levels following discontinuation of CaCO3 and resumption of aluminum gels. We conclude: (1) In addition to controlling hyperphosphatemia and increasing plasma calcium concentration, CaCO3 ameliorates metabolic acidosis. (2) Avoidance of oral aluminum intake is followed by prompt lowering of plasma aluminum levels. (3) PTH levels paradoxically increase despite the increment in plasma calcium concentration. The hypercalcemia seen with CaCO3 administration may be due, in part, to transient parathyroid hypersecretion that develops when aluminum administration is discontinued.
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PMID:Substitution of calcium carbonate for aluminum hydroxide in patients on hemodialysis. Effects on acidosis, on parathyroid function, and on calcemia. 235 86

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.
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PMID:Safety and efficacy of calcium carbonate in children with chronic renal failure. 250 75

This study evaluates the use of calcium carbonate in chronic renal failure. Forty-eight patients (25 male, 23 female, mean age 54.3 years, six pre-dialysis. 12 CAPD, 30 haemodialysis) on phosphate restriction and requiring aluminum hydroxide (mean 2.4 +/- 0.8 g/day) to control serum phosphate, were converted to an equivalent dose of calcium carbonate (2.5 +/- 0.6 g/day). None received vitamin D analogues. Three months post-conversion there was a significant decrease in mean (+/- SEM) serum phosphate (1.86 +/- 0.08 versus 1.66 +/- 0.05 mmol/l P less than 0.01) and serum aluminum (28.3 +/- 5.4 versus 13.2 +/- 3.0 micrograms/l, P less than 0.0001): calcium/phosphate product was unchanged. Post-conversion there was an increase in serum bicarbonate, (20.6 +/- 0.5 versus 22.1 +/- 0.6 mmol/l, P less than 0.01) and serum calcium (2.32 +/- 0.02 versus 2.45 +/- 0.03 mmol/l, P less than 0.0001). No change in serum creatinine, alkaline phosphatase or parathormone occurred. No adverse effects were reported but nine (18%) patients became hypercalcaemic (2.7 to 2.93 mmol/l), eight of whom responded to dose reduction. Hypercalcaemia did not correlate with pre-conversion serum calcium, parathyroid hormone, alkaline phosphatase or aluminium. Calcium carbonate is an effective alternative to aluminium-based phosphate binders. It produces a beneficial increase in serum calcium and bicarbonate and a significant decrease in serum aluminium. Hypercalcaemia is unpredictable but is easily reversible in the majority of patients.
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PMID:The use of calcium carbonate to treat the hyperphosphataemia of chronic renal failure. 251 82

Chick embryos were injected on the 14th day of incubation with 100 ng calcitriol. The concentration of Ca in their serum rose significantly 4 hours after the injection and the concentration of Pi started to decrease 10 hours after. When embryos of the same age were injected with a solution containing CaCl2, the concentrations of both Ca and P rose significantly 2 hours after the injection and remained high until the end of the experiment. The fact that both treatments produced hypercalcemia but had opposite effects on the concentration of Pi does not agree with the idea that the hypophosphatemic response to calcitriol might be secondary to the hypercalcemia which precedes it. The injection of a solution of NaHCO3 to embryos of the same age failed to produce hypophosphatemia. The fact that calcium salts and bicarbonate, when injected separately, fail to induce hypophosphatemia does not contradict the possibility that the hypophosphatemic response to calcitriol might result from the simultaneous increase in flux of Ca and -HCO3 from the shell. Three days after the injection of calcitriol to 14-day-old embryos, the total amount of Ca and P in the urine was significantly higher than in the controls. The concentration of Ca and P in kidney tissue was also significantly higher in the injected embryos. In addition, calcified precipitates were detected histochemically in the lumen of the kidney tubules from the treated embryos. These results are interpreted as demonstrating that an increase in the excretion of P in the urine is the main mechanism explaining calcitriol-induced hypophosphatemia in the chick embryo.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Role of calcitriol in phosphate regulation by the chick embryo. 254 19


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