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

Long-term CaCO3 treatment of chronic hemodialysis patients was studied. Single doses of CaCO3 were given to 25 patients, 23 of whom had been receiving Al(OH)3 before the study. When predialysis serum calcium (Ca) rose to greater than 5.5 mEq/L, CaCO3 was reduced and Al(OH)3 was administered again. Eighteen months later, serum phosphate (P) was well controlled, and predialysis serum P was less than 6.5 mg/dl in 14 patients given CaCO3 alone. Alkaline phosphatase (ALP) levels significantly decreased, and serum aluminum was remarkably lowered in patients who had discontinued Al(OH)3. In patients who resumed Al(OH)3, ALP levels rose after Al(OH)3 administration. Although levels of c-PTH did not change in CaCO3 treated patients, six patients with poor control of serum P before the study showed a significant decrease in c-PTH. These data indicate that CaCO3 is an effective P binder that stops the progression of silent osteopathy, presumably caused by oral intake of Al(OH)3, and may ameliorate these changes. However, further effort will be necessary to develop means to control serum Ca, because long-term use of CaCO3 induced hypercalcemia in half the patients.
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PMID:Long-term CaCO3 treatment of chronic hemodialysis patients: an attempt to prevent aluminum osteopathy. 319 5

Calcium citrate was evaluated as a dietary phosphate binder in 81 patients with end-stage renal disease. These patients were grouped as follows: Group 1, 43 patients who were treated with calcium citrate; and Group 2 (the control group), 38 patients who were treated with aluminum-containing compounds. Blood chemistries were measured monthly and medications adjusted to maintain the following levels: serum calcium, greater than 9 mg/dl; serum phosphorus, less than 5.5 mg/dl; and total CO2 content, greater than 22 mmol/liter. At the end of the treatment period, the following serum values were obtained in Groups 1 and 2, respectively: calcium, 9.6 +/- 1.2 mg/dl (mean +/- SD) versus 8.9 +/- 0.8 mg/dl (P less than 0.001); phosphorus 5.5 +/- 1.9 mg/dl versus 7.0 +/- 2.3 mg/dl (P less than 0.005); and calcium-phosphate product, 52 +/- 18 versus 61 +/- 21 (P less than 0.05). Differences in alkaline phosphatase, total CO2 content, and C-terminal parathyroid hormone (C-PTH) values were not statistically significant between the two groups. Fifteen patients in Group 1 were then switched to aluminum-containing compounds and chemistries were compared one month later. During calcium citrate therapy, serum calcium was significantly higher, while C-PTH and serum alkaline phosphatase were significantly reduced. No difference was noted in serum phosphorous and total CO2 content. A questionnaire completed by 17 patients in Group 1 documented excellent patient tolerance to calcium citrate. Hypercalcemia (greater than 10.5 mg/dl) was the only significant complication, but only one patient became symptomatic. We conclude that, as a phosphate binder, calcium citrate is at least as effective as aluminum-containing compounds.
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PMID:Calcium citrate, a nonaluminum-containing phosphate-binding agent for treatment of CRF. 328 Aug 55

Bone disease is recognized as a major problem in dialysis patients. initially, hyperparathyroidism was thought to be the major cause of bone disease in these patients. However, an aluminum-related bone disease has been identified in dialysis patients receiving exogenous aluminum. Patients with hyperparathyroidism and aluminum toxicity present with similar clinical and laboratory features; therefore, diagnosis of these two bone abnormalities is often difficult. Understanding normal bone development helps to elucidate the distinctions between aluminum and renal osteodystrophy. Patients with either bone syndrome may present with hypercalcemia, elevations in parathyroid hormone levels, bone pain, fractures, and radiographic evidence of subperiosteal resorption. The subtleties of these syndromes must be understood to avoid misdiagnosis. A diagnosis of hyperparathyroidism may lead to a parathyroidectomy, exacerbating the development of aluminum toxicity. Hyperparathyroidism is associated with increased surface osteoid, a high bone formation rate, increased numbers of bone cells, abnormal "twoven" osteoid, and low serum aluminum levels. Aluminum toxicity is associated with a low rate of bone turnover, paucity of bone cells, maintenance of a "laminar" osteoid, and significant aluminum bone deposition. Serum aluminum level measurements are key to the diagnosis of aluminum toxicity. For patients displaying intermediate aluminum values, the deferoxamine (DFO) challenge test is necessary for diagnosis. If noninvasive methods fail to determine a definitive diagnosis, a bone biopsy is required.
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PMID:Aluminum and renal osteodystrophy. 329 91

The efficacy of calcium carbonate (CaCO3) as a phosphate binder has been limited by its tendency to cause hypercalcemia. Since standard dialysate calcium concentrations (3.0-3.5 mEq/l) increase the risk of developing hypercalcemia with large doses of CaCO3 by inducing positive calcium balance during hemodialysis (HD), we compared control of hyperphosphatemia in 41 HD patients during 4 months each of aluminum hydroxide (Al(OH)3) and CaCO3 when the dialysate calcium concentration was lowered, as required, to maintain the predialysis serum calcium concentration within the normal range. Mean predialysis serum phosphorus and calcium concentrations were 5.0 +/- 0.2 mg/dl and 9.3 +/- 0.1 mg/dl, respectively, during 4 months CaCO3 (9.2 +/- 0.3 g/day) and 4.9 +/- 0.2 g/dl and 9.1 +/- 0.1 mg/dl during the previous 4 months Al(OH)3 therapy (2.9 +/- 0.2 g/day). Reducing the dialysate calcium concentration to below 3.0 mEq/l (mean 2.1 +/- 0.04) in the 11 patients who developed hypercalcemia on CaCO3 decreased serum calcium (-1.1 +/- 0.15 mg/dl) and ionized calcium (-0.3 +/- 0.04 mEq/l) during HD, enabled CaCO3 (8.8 +/- 0.4 g/day) to be continued, and maintained predialysis serum calcium and phosphorus at 10.4 +/- 0.1 mg/dl and 5.2 +/- 0.3 mg/dl, respectively. No improvement in acidosis or biochemical hyperparathyroidism was observed during CaCO3 therapy but serum aluminum was significantly decreased after CaCO3 (p less than 0.005). We conclude that CaCO3 prevents interdialytic hyperphosphatemia as effectively as Al(OH)3 without increasing the predialysis serum calcium x phosphorus product, provided serum calcium is maintained within the normal range by adjusting the dialysate calcium concentration.
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PMID:Calcium carbonate is an effective phosphate binder when dialysate calcium concentration is adjusted to control hypercalcemia. 342 32

We report on a 5-year, prospective, double-blind trial of 1,25 dihydroxycholecalciferol (calcitriol) versus placebo in 76 hemodialysis patients without biochemical or radiological evidence of bone disease. Calcitriol, 1 microgram daily, regularly induced hypercalcemia. Doses of 0.25 microgram daily or less proved satisfactory in most patients. During calcitriol treatment, plasma calcium concentration was significantly higher and serum parathyroid hormone concentration significantly lower than on placebo. There was no difference in the rates of development or of progression of vascular calcification in the two groups. Significantly more patients on placebo (17 vs. 6, p less than 0.05) developed a sustained elevation of plasma alkaline phosphatase concentration. Calcitriol appeared to protect against the development of histological evidence of osteitis fibrosa but not of osteomalacia, but accumulation of aluminum in bone occurred during the study. We conclude that calcitriol delays and may prevent the development of osteitis fibrosa in patients receiving regular hemodialysis and may reasonably be prescribed routinely in hemodialysis patients without biochemical or radiological abnormality, unless there is a substantial prospect of early renal transplantation.
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PMID:Controlled trial of calcitriol in hemodialysis patients. 353 32

The present study evaluates the effect of an intravenous (i.v.) aluminum infusion on total and ionized calcium. Seven groups of rats were studied, and it was found that the magnitude of hypercalcemia was dose dependent. During a two hour i.v. infusion containing 0.4 mg aluminum per 100 grams of body weight, the total plasma calcium increased from 9.7 +/- 0.2 to 12.7 +/- 0.7 mg/dl (X +/- SE, P less than 0.02) while the ionized calcium decreased from 5.1 +/- 0.12 to 4.05 +/- 0.24 mg/dl (P less than 0.001). The increase in plasma calcium occurred in intact and parathyroidectomized rats, and the hypercalcemia could not be attributed to changes in PTH, arterial pH, plasma protein, or plasma phosphate. In vitro studies indicate that the addition of aluminum to rat plasma results in decreased ionized calcium concentration. Similarly, ultrafilterable calcium declined from 5.4 +/- 0.17 to 4.53 +/- 0.12 mg/dl (P less than 0.001) after the addition of aluminum to rat plasma. In summary, high levels of intravenous aluminum increase total plasma calcium and decrease ionized calcium. As also supported by in vitro data, the most probable mechanism is increased binding of calcium in the plasma which decreases ionized calcium. As a result of the decreased concentration of ionized calcium, movement of bone and interstitial calcium into the vascular space may occur, thus increasing total plasma calcium.
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PMID:The role of aluminum in the development of hypercalcemia in the rat. 357 39

Traditionally, phosphate binders containing aluminum have been used effectively to control serum phosphorus levels in patients with chronic renal failure. In these patients, however, absorption and accumulation of aluminum in plasma and tissues can lead to debilitating pathologic conditions, including aluminum-related osteodystrophy. An alternative therapeutic approach using calcium carbonate as a phosphate binder has been proven to be effective. In a recent study of 20 patients on chronic hemodialysis, the efficacy of calcium carbonate therapy was demonstrated. Serum phosphorus levels in these patients were 4.8 +/- 0.13 mg/dL with the use of aluminum-containing phosphate binders, 7.3 +/- 0.26 mg/dL when phosphate binders were discontinued, and 4.8 +/- 0.17 mg/dL with the use of calcium carbonate (Os-CaL 500) therapy. The total amount of aluminum ingested for all 20 patients combined went from 112 g/d at the beginning of the study to 22 g/d at the end of the study. The amounts of calcium carbonate administered varied because of large variations in dietary phosphorus intake between patients. In addition, the individual distribution of phosphorus intake during the day dictated the dosing schedule. There were no adverse side effects associated with calcium carbonate therapy. A few patients ingesting large amounts of calcium carbonate to control their extremely high phosphorus levels developed hypercalcemia. However, this effect was reversible after discontinuation of calcium carbonate therapy.
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PMID:Alternative phosphate binders in dialysis patients: calcium carbonate. 360 77

45 bone biopsies from patients with chronic uremia were reviewed to define which noninvasive investigations were of value in predicting the histological diagnosis and to quantify the spectrum of uremic bone disease at a center that has consistently used an aluminum-free dialysis bath. 17 biopsies were taken postmortem. 15 patients received conservative treatment, the rest were on maintenance dialysis. 13 patients had symptomatic bone disease. Virtually all patients with a uremia duration greater than 3 years had uremic osteodystrophy. All patients with clinical bone disease, hypercalcemia or raised alkaline phosphatase activity had osteodystrophy, but the specific histology was not indicated. Greatly raised parathyroid levels suggested secondary hyperparathyroidism, but the test was only 100% specific when 20 times normal. Total aluminum consumption was highly indicative of bone aluminum concentration (p less than 0.0001) and aluminum-related osteomalacia (5 cases), suggesting that a considerable proportion of uremic bone disease is iatrogenic. Serum aluminum was of some use in the diagnosis of aluminum-related osteomalacia, but was not wholly reliable. Bone mineral content (BMC) using both forearm measurements and total body bone mineral levels (TBBM) were assessed in 32 patients and were found to be reduced in 12, with a preponderance of secondary hyperparathyroidism. BMC and TBBM were negatively correlated to resorbing surfaces and bone formation rate, suggesting that secondary hyperparathyroidism is the uremic bone disease that represents the greatest threat to bone mass. It is concluded that while noninvasive investigations give considerable information, reliable diagnosis requires the use of histological methods.
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PMID:Noninvasive diagnosis of uremic osteodystrophy: uses and limitations. 363 Nov 50

This study was undertaken to determine the success of surgical treatment of advanced secondary (renal) hyperparathyroidism. From 1978 to 1985, total parathyroidectomy and autotransplantation (TPA) were performed for secondary hyperparathyroidism in 23 patients who had had dialysis for a mean of 6.5 years preoperatively. Indications for surgery included hypercalcemia, bone pain and pathologic fractures, metastatic calcification, and pruritus. Four glands were found and removed in all patients; 100-150 mg of diced tissue were autotransplanted to one forearm. Two patients died of myocardial infarction in the first postoperative week. Bone pain, present in 19 of 23 patients, was relieved almost immediately postoperatively and relief was sustained to death (of unrelated causes) or most recent follow-up in 13 patients. All fractures healed. All patients had markedly elevated serum parathormone (PTH) preoperatively and 14 of 23 were hypercalcemic. The group mean values of serum calcium, alkaline phosphatase, and PTH all fell to and remained in a normal range by 1 year postoperatively in that subset of patients who did not suffer recurrence. Six patients were reoperated on after 12 to 37 months with partial graft excision for recurrent bone pain and hypercalcemia. Bone pain in two of these patients was due to aluminum-associated bone disease and the diagnosis of recurrent secondary hyperparathyroidism was erroneous. The actual recurrence rate was thus 19 per cent. Consistent technical success, with no late hypocalcemia, was achieved and most patients were restored to medical manageability.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A community hospital experience with total parathyroidectomy and autotransplantation for renal hyperparathyroidism. 368 58

Orally administered calcium carbonate was evaluated as a phosphate binding agent in 15 children, ages 0.6 to 17.2 years, receiving maintenance dialysis. Changes in plasma aluminum concentration were assessed after discontinuation of treatment with aluminum-containing gels. The mean daily dose of calcium carbonate was 5.1 +/- 2.5 gm (384 +/- 315 mg/kg/day), and correlated inversely with body weight (r = 0.72, P less than 0.01) and age (r = 0.71, P less than 0.01). Mean serum calcium, phosphorus, and bicarbonate values were unchanged throughout the study. Plasma aluminum concentration fell from 90 +/- 51 to 34 +/- 22 micrograms/L (P less than 0.005). Dietary phosphorus intakes were 44 +/- 21 and 42 +/- 19 mg/kg/day during the control period and at the end of the study, respectively. Transitory hypercalcemia was the only side effect in 92% of the patients. In none of the patients did uncontrolled hyperphosphatemia, metabolic alkalosis, diarrhea, or symptoms or signs of hypercalcemia develop. Our data indicate that calcium carbonate is an effective phosphate binding agent in children receiving dialysis, and should be used in lieu of aluminum-containing gels in young children with renal failure.
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PMID:Effects of oral calcium carbonate on control of serum phosphorus and changes in plasma aluminum levels after discontinuation of aluminum-containing gels in children receiving dialysis. 370 25


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