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

With increasing recognition of problems regarding the use of aluminum hydroxide as a phosphate binder, calcium carbonate has become the medication of choice. Use of calcium has, however, frequently been associated with development of hypercalcemia. At this institution, calcium carbonate powder as a phosphate binder, examination of its efficacy, and the frequency of hypercalcemia with its use were of great interest. Calcium carbonate powder (CalCarb-HD, 2.4 gms elemental calcium/packet) (CalCarb-HD, Lafayette Pharmacal Inc., Fort Worth, TX) was used in the study. Twenty-one end-stage renal disease (ESRD) patients (17 hemodialysis and 4 chronic ambulatory peritoneal dialysis) were chosen and converted from their previous binder (primarily, calcium carbonate tablets) to calcium powder. The dosage was adjusted to keep phosphorus levels at 3.5 to 5.5 mg/dl and calcium less than 11.5 mg/dl. At 2 months, the average calcium level in the 16 patients remaining in the study was 9.2 mg/dl, and the average phosphorus level was 5.2 mg/dl with an average calcium dose of 1.4 packets/day. By 7 months, the 8 patients remaining in the study had an average calcium level of 9.9 mg/dl with an average phosphorus level of 5.5 mg/dl; average calcium dose was 1.8 packets/day. Total episodes of hypercalcemia (calcium greater than 11.5 mg/dl) were two. Calcium carbonate powder appears to be an effective phosphate binder in the ESRD population. The relatively few episodes of hypercalcemia may be related to possible enhanced bioavailability of the compound secondary to its powdered form.
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PMID:Calcium carbonate powder as a phosphate binder. 259 73

Many investigators have shown that calcium carbonate (CaCO3) is an effective phosphate binder which also prevents the potential disabling effects of aluminum (Al) accumulation. However, hypercalcemia may develop in a substantial numbers of patients. Thus, to control serum phosphate (PO4) and prevent hypercalcemia, we performed studies in 21 patients on maintenance hemodialysis in which, in addition to the oral administration of CaCO3, the concentration of calcium (Ca) in the dialysate was reduced from 3.25 to 2.5 mEq/liter. The studies were divided in three periods: I. control, on Al-binders (one month); II. no Al-binders (one month); III. CaCO3 (seven months). Blood was obtained three times/week before dialysis for the first five months of the study and once a week for the remaining four months. During the control period, the mean serum calcium was 8.86 +/- 0.08 mg/dl. The value decreased to 8.65 +/- 0.07 mg/dl when phosphate binders containing aluminum were discontinued, and increased to 9.19 +/- 0.07 mg/dl (P less than 0.001 compared to period II) during oral supplementation with calcium carbonate. The mean serum phosphorus was 5.03 +/- 0.07 mg/dl during the control period, and increased to 7.29 +/- 0.91 mg/dl (P less than 0.001) after phosphate binders were discontinued. It decreased to 4.95 +/- 0.06 mg/dl (P less than 0.001) with the administration of calcium carbonate. During CaCO3 administration, serum Al decreased from 64.2 +/- 8.5 to 37.1 +/- 3.6 and 25.1 +/- 3.0 micrograms/liter (P less than 0.001) at three and seven months, respectively. Serum parathyroid hormone (PTH) decreased by 20%.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Long-term effects of calcium carbonate and 2.5 mEq/liter calcium dialysate on mineral metabolism. 261 97

The mechanism of stone formation in the urinary tract is reviewed. Diet, urinary tract infection and metabolic disorders account for the different epidemiological patterns of stone formation. The diagnosis and management of renal tract calculi are discussed. Calcium stones are associated with hypercalciuria, urine acidification defects, the use of furosemide in premature babies, hypercalcaemia, hyperoxaluria, hyperuricosuria, an alkaline urine and hypocitraturia. Uric acid stones occur in acid urine, from increased purine synthesis with lympho- or myeloproliferative disorders or from several inborn errors of purine metabolism which can also cause xanthine or dihydroxyadenine stones. Cystinuria, inherited as an autosomal recessive disorder is best treated with a low sodium diet, a fluid intake exceeding 40 ml/kg per day maintaining urine pH between 7.5 and 8 and, if necessary, with oral penicillamine. Oxalate stones occur in relation to diet, bowel disease and primary inherited defects in oxalate metabolism. Urinary tract infection causing struvite and carbonate apatite formation is the commonest cause of stones in Europe.
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PMID:Urolithiasis in children: current medical management. 270 15

A calcium-free, bicarbonate-containing concentrate was prepared for hemodialysis, which, after dilution, gave analyzed concentrations of sodium of 146 mmol/l, Cl 110 mmol/l, HCO3 of 35 mmol/l and pH of 8.3. When compared with standard bicarbonate dialysis, no important differences in blood chemistries, symptoms or signs were seen. The solution has been trouble-free in over 300 dialyses. Total amount of calcium lost uncorrected for time, dialyzer or blood flow was 40.6 +/- 1.1 mmol, n = 62. This loss was replaced by a calcium infusion into the venous line giving 40 mmol calcium over 4 h. The dialyzate calcium loss could be accurately predicted by sampling without collecting the total dialyzate volume. The uses of this concentrate for bicarbonate dialysis, citrate anticoagulation and avoidance of hypercalcemia in patients treated with oral calcium for phosphate binding is discussed.
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PMID:Calcium-free dialyzate: development and applications. 270 10

Aluminium-containing phosphate binders were replaced by a calcium and magnesium carbonate-containing antacid in 20 patients on long-term haemodialysis, over a three-month period in all of them, for 12 months in ten. After two months the serum aluminium level fell (mean +/- SD) from 3.0 +/- 1.6 to 1.4 +/- 0.5 mumol/l (P less than 0.001). After three months the serum phosphate level had fallen from 1.8 +/- 0.4 to 1.5 +/- 0.4 mumol/l (P less than 0.05), while during the same period parathormone (PTH-NH2) fell from 1.4 +/- 1.4 to 0.8 +/- 0.7 ng/ml (P less than 0.05). Serum total calcium concentration rose after two months from 2.2 +/- 0.2 to 2.4 +/- 0.2 mmol/l (P less than 0.001). In a third of patients the uraemic acidosis was corrected, standard bicarbonate rising from 18 +/- 2 to 21 +/- 3 mmol/l (P less than 0.05). Serum pH, potassium, sodium, magnesium and alkaline phosphatase did not change significantly. Hypercalcaemia was an expected disadvantage: repeated symptom-free episodes of hypercalcaemia occurred in six of 20 patients during the first three months and in a further two up to 12 months. These episodes were successfully controlled by a reduction of CaCO3/MgCO3 dosage and readministration of Al(OH)3. Extraosseous calcifications were not observed.
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PMID:[Replacement of aluminum-containing phosphate binders by calcium and magnesium carbonates in long-term hemodialysis]. 270 34

Calcium salts are increasingly used as phosphorus binders in patients with chronic renal failure. Calcium carbonate is the principal salt presently utilized, however, other calcium salts may be more effective and safer phosphorus binders. Theoretical calculations, in vitro experiments, and in vivo studies in normal subjects have shown calcium acetate to be a more effective phosphorus binder than other calcium salts. This salt has not previously been studied in patients with chronic renal failure. We used a one-meal gastrointestinal balance technique to measure phosphorus absorption, calcium absorption and phosphorus binding in six patients with chronic renal failure. Calcium acetate was compared with calcium carbonate and placebo. Equivalent doses (50 mEq Ca++) of calcium acetate bound more than twice as much phosphorus (106 +/- 23 mg) as calcium carbonate (43 +/- 39 mg) P less than 0.05. When phosphorus binding was factored for calcium absorption, calcium acetate bound 0.44 mEq HPO4 =/mEq absorbed Ca++ compared with 0.16 mEq HPO4 = bound/mEq Ca++ absorbed with calcium carbonate. More efficient phosphorus binding permits serum phosphorus concentration to be controlled with lower doses of calcium salts. The higher phosphorus binding/calcium absorption ratio coupled with a lower dose indicates that less calcium will be absorbed when calcium acetate is used for phosphorus control. Markedly positive calcium balance, hypercalcemia and ectopic calcification should be less likely to occur with this drug than other calcium salts.
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PMID:Calcium acetate, an effective phosphorus binder in patients with renal failure. 281 Oct 66

Renal failure is frequently associated with osteodystrophia due to secondary hyperparathyreoidism and/or increased aluminum intake. The problem of hypercalcemia and hyperphosphatemia can more easily controlled by CAPD than by hemodialysis. Total serum and ionized calcium levels are rapidly normalized by a CAPD regime of four 2-1 exchanges with 1.75 mmol/l Ca. Under the same CAPD regime 250-300 mg phosphate are removed per day. Depending on the ingestion of phosphate, 100-200 mg phosphate per day remain to be removed by phosphate binding agents. Since the main source of aluminum in CAPD patients is oral ingestion of aluminum-containing phosphate binders, serum levels should be regulated by diet and calcium carbonate. To suppress PTH secretion serum ionized calcium levels need to be maintained at the upper limit of normal. This can also be achieved by the use of oral calcium carbonate. Vitamin D or analogs should be prescribed only when clinically indicated by persistent hypocalcemia, osteitis fibrosa or non-aluminum related osteomalacia.
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PMID:Renal osteodystrophy and aluminum bone disease in CAPD patients. 305 62

The hypothesis that chronic metabolic acidosis encountered in some patients with primary hyperparathyroidism is due to inhibition of proximal HCO3 reabsorption has recently been challenged. Indeed, this action of parathyroid hormone (PTH) has only been observed in acute studies, whereas in animal models of chronic hyperparathyroidism a metabolic alkalosis has been induced, probably owing to the release of alkaline salts from bone tissue, and to the stimulation of tubular acid secretion by hypercalcaemia. Studies were, therefore, performed to determine the effect of PTH on the renal handling of HCO3 in an animal model in which changes in plasma calcium and phosphate, and nephrocalcinosis, all known to affect tubular acidification, did not occur. Thyroparathyroidectomized (TPTX) rats were infused with synthetic bovine hormone fragment bPTH 1-34 via Alzet minipumps at the rate of 0.7 U h-1 to simulate normal endogenous production of PTH (group I) and at the three-fold higher rate of 2.1 U h-1 (group II). In order to prevent changes in serum calcium and phosphate, and nephrocalcinosis, animals of group II were fed a Ca- and P-free diet prior to TPTX (compared with a regular diet for group I) and both groups were treated with dichloromethylene-diphosphonate (Cl2MDP, 10 mg kg-1 day-1) and a Ca-free diet during PTH infusion. During the course of PTH infusion both groups of animals had stable and normal levels of plasma calcium and phosphate.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Parathyroid hormone directly inhibits tubular reabsorption of bicarbonate in normocalcaemic rats with chronic hyperparathyroidism. 312 45

The efficacy and safety of calcium carbonate as a phosphate binder was evaluated in 20 patients on chronic hemodialysis who had previously received aluminum hydroxide. During the control period the patients were on aluminum hydroxide and calcitriol therapy and had plasma phosphorus levels less than 6 mg/dL (4.95 +/- 0.8 mg/dL). Aluminum hydroxide was then discontinued and no phosphate binder was prescribed for 1 month. Every patient developed hyperphosphatemia so that calcium carbonate treatment was begun and calcitriol dose was adjusted in relation to plasma calcium changes. After 24 months of calcium carbonate therapy, plasma phosphorus was 4.85 +/- 0.7 mg/dL, using a daily dose of calcium carbonate of 2.57 +/- 1.3 g (range, 1 to 6 g). The daily dose per patient of calcitriol was not different from that prescribed during the control period, but in five patients calcitriol was permanently withdrawn for hypercalcemia. At the end of the study plasma calcium, magnesium, bicarbonate, alkaline phosphatase, and parathyroid hormone values were unchanged in comparison with the control period, whereas a significant reduction in plasma aluminum and plasma aluminum increase induced by deferoxamine infusion was observed. The frequency of hypercalcemic and hyperphosphatemic episodes during the last 12 months of calcium carbonate therapy (6.2% and 16.6%, respectively) was not different from that observed during the 12 months on aluminum hydroxide therapy preceding the control period (4.5% and 14.7%, respectively). It was concluded that calcium carbonate is effective in the control of hyperphosphatemia and secondary hyperparathyroidism in patients on chronic hemodialysis and that the incidence of hypercalcemia is low when the daily dosage is less than 6 g.
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PMID:Efficacy and safety of long-term treatment with calcium carbonate as a phosphate binder. 314 60

Recurrent and unusually severe hypercalcemia was observed in an infant undergoing continuous cycling peritoneal dialysis and receiving oral calcitriol and calcium carbonate. Rapid correction was achieved with peritoneal dialysis using a calcium-free dialysis solution.
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PMID:Treatment of severe hypercalcemia with peritoneal dialysis in an infant with end-stage renal disease. 315 36


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