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

We evaluated musculoskeletal complaints related to arthropathy in 28 patients with end stage renal failure receiving maintenance dialysis. Twenty-three of 28 patients had arthritic complaints and 14 had an arthropathy. Six of 14 patients with arthropathy had a pattern resembling calcium pyrophosphate dihydrate deposition (CPPD) disease, 4 patients had moderately severe osteoarthritis, 3 had calcific periarthritis, and 1 patient had acute arthritis with intermittent pain and swelling. Factors which predispose to metabolic arthropathies were observed as follows: 29% elevated ferritin; 39% history of hyperparathyroidism; 68% elevated parathormone; 54% hyperphosphatemia; 36% hypercalcemia, 29% HLA haplotypes A3, B7, or B14; and 60% hyperaluminemia. The arthropathy group had more abnormalities per patient (mean 3.6) than the group without arthropathy (mean 2.7) (p less than 0.05). Our data suggest that (1) arthritic complaints occur frequently in patients receiving dialysis; (2) arthropathy accounted for 61% of the complaints; (3) 43% of patients with arthropathy had CPPD-type; (4) renal osteodystrophy caused 17% of arthritic complaints; and (5) in patients receiving dialysis, there is a high incidence of metabolic abnormalities that are known to be associated with arthropathy.
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PMID:Musculoskeletal symptoms related to arthropathy in patients receiving dialysis. 323 May 70

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

Radionuclide imaging with Tc-99m diphosphonates is not an effective method for detecting or ruling out most osteoporotic diseases including senile osteoporosis or accelerated postmenopausal osteoporosis, and the slow loss of bone tissue generally remains undetected by this modality. Nonetheless, it frequently surpasses or supplements radiographic findings in evaluating the focal complications of metabolic bone disease, including fractures, microfractures, stress fractures, vertebral compressions, Milkman-Looser zones, aseptic necrosis, and acute infarction. In contrast to its secondary role in osteoporosis, bone imaging is of prime importance in investigating hypercalcemia, because the major cause of this abnormality is skeletal metastatic malignancy. In defective bone mineralization due to hyperparathyroidism or osteomalacia, a general increase in diphosphonate skeletal uptake is detected more frequently than radiographic abnormalities. However, normal skeletal images do not rule out metabolic bone disease. Biochemical testing is more reliable in detecting primary hyperparathyroidism. On the other hand, in renal osteodystrophy, biochemical abnormalities are variable and bone imaging is helpful in assessing the severity of skeletal involvement, but not its etiology. Many methods of quantitating the kinetics of Tc-99m diphosphonates have been explored, such as plasma clearance, bone-to-soft-tissue ratios, 24-hour total body retention and 24-hour urinary excretion. None of these have been widely accepted. The value of bone imaging is established in other systemic diseases, most notably in Paget's disease, hypertrophic pulmonary osteoarthropathy, sickle cell disease, fibrous dysplasia, and sympathetic dystrophy.
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PMID:Radionuclide imaging in metabolic and systemic skeletal diseases. 331 47

During maintenance hemodialysis in patients with chronic renal failure, acute elevations of the plasma calcium are common, although of doubtful significance. Because the mechanisms for this hypercalcemia are unclear, calcium, magnesium, and inorganic phosphate mass transfer data was collected during routine hemodialysis. While the increase in the plasma calcium did not significantly correlate with the gain of calcium from the dialysate nor with the dialysate calcium concentration, there was a significant positive correlation between the degree of hypercalcemia and the loss of body phosphate (r = 0.66, P less than 0.05, n = 15). Hemodialysis without ultrafiltration and concomitant hemoconcentration depressed the dialysis hypercalcemia by 46% (P less than 0.001). However, continuous infusion of 33.5 mmol of phosphate during a 5-hour dialysis period, which reduced the plasma phosphate fall (1.53 +/- 0.16 to 0.87 +/- 0.08 mmol/L, P less than 0.01, in the control group; compared with 1.59 +/- 0.19 to 1.35 +/- 0.11 mmol/L, not significant [NS], in the phosphate infusion group) abolished the hypercalcemia (2.38 +/- 0.07 to 2.54 +/- 0.04 mmol/L, P less than 0.01, in the control group and 2.39 +/- 0.06 to 2.41 +/- 0.04 mmol/L, NS, in the phosphate infusion group). It is suggested that during routine hemodialysis, the loss of inorganic phosphate from the body is excessive, and that phosphate as well as calcium is released from the intracellular pool in response to the rapid fall in the plasma phosphate concentration. Such rapid, repetitive, and excessive losses of phosphate, particularly from bone, may be an important cause of renal osteodystrophy.
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PMID:Acute dialysis hypercalcemia and dialysis phosphate loss. 336 42

High doses of calcitriol were used prospectively for 11 to 29 months to raise serum calcium levels in an effort to control renal osteodystrophy in 16 children undergoing CAPD. Serum Ca, P, iPTH and alkaline phosphatase were measured monthly; hand radiographs were obtained every six months, and a semiquantitative score of bone abnormalities was evaluated by two independent observers. During the study, serum Ca increased from 9.9 +/- 0.9 to 11.0 +/- 0.6 mg/dl (P less than 0.001); serum iPTH decreased by 113 +/- 131 microliter Eq/ml (P less than 0.005); serum P was unchanged; and serum alkaline phosphatase fell by 33 +/- 46% (P less than 0.02), 530 +/- 397 to 204 +/- 551 IU/liter. The radiographic score fell from 4.8 +/- 4.6 to 0.9 +/- 1.2 (P less than 0.005). The average and maximal doses of calcitriol were 0.61 +/- 0.37 and 0.95 +/- 0.56 microgram/day or 28 +/- 18 and 46 +/- 28 ng/kg body wt/day, respectively. Transient and asymptomatic hypercalcemia occurred in nine patients and two patients had reversible conjunctivitis in association with the hypercalcemia. Thus, "high dose" calcitriol prevented or controlled progression of hyperparathyroid bone disease in most pediatric CAPD patients. The failure to suppress PTH or reverse secondary hyperparathyroidism until the serum Ca rose to 10.5 to 11.0 mg/dl could reflect an increase in the "set point" for PTH suppression by serum calcium in many uremic children.
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PMID:"High-dose" calcitriol for control of renal osteodystrophy in children on CAPD. 362 2

In view of the known toxicity of aluminum, we studied the effects of CaCO3 as an alternative phosphate binder in 12 chronic renal failure (CRF) children during 152 patient-months. Mean (+/- SD) serum creatinine concentration rose during that period from 3.7 +/- 1.8 to 5.1 +/- 3.0 mg/dl. 8 patients received CaCO3 from the start, and 4 were switched from A1(OH)3 after 2 months of interruption. In addition to CaCO3 (0.1-0.3 mg/kg BW) all patients received NaHCO3, and all but two received 1 alpha-hydroxyvitamin D3 [1 alpha(OH)D3] or dihydrotachysterol (DHT). Urine and blood variables were checked every 4-6 weeks and medication dosages were adjusted accordingly, aiming to keep serum Ca at 10.4-10.8 mg/dl, serum Pi at 3.5-5.5 mg/dl, and serum HCO-3 above 18 mEq/l. Bone X-rays were obtained every 6-9 months. With treatment, mean serum Ca increased from 8.9 +/- 0.7 to 10.3 +/- 0.4 mg/dl (p less than 0.01), serum Pi decreased from 6.3 +/- 0.9 to 4.2 +/- 0.5 mg/dl (p less than 0.01), and the mean Ca X P product decreased slightly and insignificantly. Mean serum alkaline phosphatase levels decreased significantly from 486 +/- 251 to 168 +/- 28 IU (p less than 0.01). Bone X-rays at the end of the study showed either healing of renal osteodystrophy or its prevention. Only one episode of mild hypercalcemia (serum Ca 11.7 mg/dl) was observed in 1 patient, but his Ca X P product remained low.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Oral calcium carbonate as phosphate-binder in infants and children with chronic renal failure. 380 30

Ten dialysis-treated patients with hypercalcemia (11.5 +/- 0.3 mg/dl, mean +/- SE) due to renal osteodystrophy were compared with 30 control dialysis-treated patients who were not hypercalcemic (9.5 +/- 0.1 mg/dl). The hypercalcemic patients were more disabled than the control patients. Fifty percent of the hypercalcemic patients and 37 percent of the control patients had a mineralization defect (p greater than 0.6). In the control group, intact parathyroid hormone level was significantly higher in patients with osteitis fibrosa than in those with osteomalacia (247 +/- 39 pg/ml versus 60 +/- 20 pg/ml, respectively, p less than 0.005) whereas in the hypercalcemic patients, parathyroid hormone measurements did not discriminate between these two types of bone disease. Osteomalacia was more severe and bone aluminum staining was stronger in the hypercalcemic patients than in the control patients (2.02 +/- 0.47 versus 0.35 +/- 0.11 mm/mm2 tissue area, p less than 0.001). The mean serum calcium level fell from 11.2 +/- 0.2 mg/dl to 10.5 +/- 0.3 mg/dl (p less than 0.01) in eight hypercalcemic patients treated with 24,25-dihydroxyvitamin D. It is concluded that hypercalcemia in patients undergoing dialysis is associated with an increase in bone aluminum level, and with more severe osteomalacia. Intact parathyroid hormone levels are useful for predicting bone histomorphometric parameters but only when hypercalcemia is not present. The drug, 24,25-dihydroxyvitamin D, was effective in lowering the serum calcium level.
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PMID:Spontaneous hypercalcemia in patients undergoing dialysis. Etiologic and therapeutic considerations. 396 41

Seven patients with advanced renal failure, six of whom were dialysed, received a cation exchange resin in the calcium cycle because of severe hyperkalemia, together with their usual preventive treatment of renal osteodystrophy, including 25 hydroxycholecalciferol. Hypercalcemia developed in four subjects within less than thirty days and disappeared within four days following the withdrawal of the resin. Patients who exhibited hypercalcemia had higher calcium intake, lower predialysis blood calcium and higher PTH values before introduction of the treatment. Three of the four hypercalcemic patients were diabetics. It is therefore advised to frequently monitor blood calcium when using calcium exchange resin in patients treated with vitamin D analogs.
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PMID:Hypercalcemia in 25 OH D3 treated patients receiving a calcium exchange resin. 401 32

A method is described for the quantitation of total skeletal activity during bone scans. The method requires a single plasma sample only, taken at the time of imaging. The ratio of % injected dose of 51Cr EDTA to that of 99Tcm MDP is calculated from this sample following combined injection of the two radiopharmaceuticals. The 51Cr EDTA level corrects for the glomerular filtration of 99Tcm MDP. Using this method, which only requires a gamma counter, significant differences from normal controls have been shown in patients with osteomalacia, renal osteodystrophy, Paget's disease and hypercalcaemia. The method provides routine quantitative data to add to the imaging information in the bone scan.
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PMID:Chromium 51 EDTA/technetium 99m MDP plasma ratio to measure total skeletal function. 623 85

Growth arrest and renal osteodystrophy is a major problem in renal insufficiency of children. The present report describes our experiences in managing renal osteodystrophy by using vitamin D3 for 24 months. Values in plasma of Ca, Mg, alkaline phosphatase, iPTH, 25-OH-D were determined regularly. Skeletal X-rays and analysis of iliac crest bone biopsies were obtained in each child. In treatment with vitamin D3 no hypercalcemia was seen despite high serum levels of 25-OH-D. Plasma-Ca, alkaline phosphatase, and iPTH normalized nearly. Radiographic abnormalities improved. Bone biopsies showed improvement in signs of secondary hyperparathyroidism and ostitis fibrosa, whereas osteomalacia remained unchanged. Osteoblast population showed a small reduction. No real increment in body growth was seen.
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PMID:[Influence of vitamin D therapy on renal osteodystrophy in children (author's transl)]. 624 57


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