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

Female Sprague-Dawley rats (100-120 g) were kept for 12 d on diets containing 250, 1500, or 9000 ppm Mg. Then subgroups were loaded with water, frusemide or magnesium and urine was collected over 6 h. Moderately Mg-deficient diet (250 ppm) induced moderate hypomagnesaemia (62.3% of controls), but did not result in hypercalcaemia or the formation of typical erythema. Nevertheless, pronounced nephrocalcinosis developed, as shown by increased renal wet and dry weight and elevated tissue concentrations of Ca, P and Mg, the calculous deposits probably consisting to a large extent of Ca3 (PO4)2. Despite these alterations, renal function remained unimpaired in Mg-deficient rats, as shown by normal urinary creatinine excretion and the unaffected ability of the kidneys to concentrate urine. Loading with water, frusemide or Mg increased urinary excretion of calcium in all three diet groups to a similar extent; hence no significant proof can be given that calculous deposits are mobilized under these conditions. Since comparable conditions may also be present under clinical conditions in man, special care should be given to maintain optimal Mg balance.
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PMID:Nephrocalcinosis without functional renal impairment in rats subjected to subacute moderate magnesium deficiency, and intervention studies on the mobilization of calcium deposits. 213 28

Three siblings with neonatal familial hyperparathyroidism diagnosed at age 4 months, 2 months, and 5 days, respectively, were treated. Hypercalciuria, nephrocalcinosis, and renal tubular acidosis were present in each child. In all three, there were higher responses of serum parathyroid hormone to serum calcium and higher elevation of serum calcium with oral calcium loading. The metabolism of vitamin D and calcitonin seemed to be intact. Hypercalcemia associated with the abnormal response of parathyroid hormone secretion disappeared when the children passed the age of approximately 2 years, although renal tubular acidosis and nephrocalcinosis remained. An autosomal recessive inheritance seems likely.
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PMID:Self-limited neonatal familial hyperparathyroidism associated with hypercalciuria and renal tubular acidosis in three siblings. 216 60

The phenomenon of calciphylaxis as defined by Selye is a condition of hypersensitivity that results in acute local calcification of various organs, with a whole host of morbid processes. Nephrocalcinosis and cutaneous calcifications have long been recognized in patients with chronic renal failure, but they have not often been reported in acute hyperparathyroidism or other causes of calcium-phosphate metabolism aberrations. The pathogenesis is not clear, and both the sensitizer and challenging agent in the hypersensitivity theory are often elusive, though hypercalcemia is the most consistent factor. The clinical features vary according to the organs affected and often mimic a gamut of more common conditions. Treatment is primarily supportive, with specific measures only possible when a sensitizer or challenger is identified. Correction of the hypercalcemia is, however, imperative. It is important to recognize this rare condition to avoid the more serious end results often reported.
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PMID:Calciphylaxis and systemic calcinosis. Collective review. 218 92

An ongoing randomized clinical trial of 3 years duration is being undertaken to evaluate the recurrent fracture rate and safety profile associated with low-dose calcitriol versus calcium supplementation in women with at least 3 years postmenopausal osteoporosis who are under the age of 80 years. A total of 856 patients were submitted for possible inclusion in the study by 123 primary care physicians, and 636 met all entry requirements. Each patient was randomly allocated to receive either 0.25 micrograms of calcitriol twice daily or calcium supplementation of 1,000 mg/d. If significant hypercalcemia developed (greater than 2.6 mmol/L) or a deterioration in renal function was observed, the dose of trial medication was to be halved or stopped if laboratory values did not return to normal. Patients were given no specific instructions regarding dietary calcium intake. To date, 528 patient-years experience with calcitriol and 527 patient-years experience with calcium the calcium supplementation have been accumulated. Thus far, low-dose calcitriol has not been observed to cause hypercalcemia, deterioration in renal function, or nephrocalcinosis. At 1 year, a loss in total anterior height (P less than .05) has been detected in the calcium-treated group compared with the calcitriol-treated group. Thus, calcitriol appears to preserve spinal height. Long-term follow-up of all patients for 2 or 3 years will be continued.
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PMID:Low-dose calcitriol versus calcium in established postmenopausal osteoporosis. 232 72

The relationship of sarcoidosis to renal insufficiency is not widely known by pathologists or clinicians. During an 8-year period beginning in 1980, we observed six patients with sarcoidosis and clinically significant renal insufficiency (serum creatinine, greater than 260 mumol/L). In one of these patients with long-standing sarcoidosis, renal insufficiency was attributed to unrelated primary renal disease until renal biopsy specimen showed interstitial noncaseating granulomas. The four patients with renal insufficiency at presentation differed from the typical patient with sarcoidosis because they were white men who lacked the usual clinical constellation of skin, eye, and pulmonary involvement. All four had noncaseating granulomas on their initial biopsy (bone marrow [3 patients], and lymph node [1 patient]), suggesting each had sarcoidosis, yet each had two or more follow-up biopsies before the diagnosis of sarcoidosis was accepted and appropriate therapy initiated. One of these four patients underwent long-term antifungal and antituberculous therapy. The major causes of renal insufficiency in these six patients were complications of hypercalcemia and interstitial granulomatous nephritis. Except in one patient with nephrocalcinosis, prednisone therapy resulted in a dramatic fall in serum creatinine level with resolution of hypercalcemia. Sarcoidosis is a rare, but treatable, cause of renal insufficiency. Early recognition by clinicians and pathologists may spare patients from undergoing unnecessary biopsies and result in more timely initiation of therapy.
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PMID:Renal insufficiency in sarcoidosis. A clinical and pathologic study. 233 57

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

The effect of dietary phosphorus (P) on calcium (Ca) and phosphorus metabolism was studied in young female rats. P levels in the semipurified diets ranged from 0.1 to 0.4% (w/w). A level of 0.4% P in the diet is recommended for rats. Kidney calcification was observed in rats fed the 0.4%-P diet whereas P restriction prevented this condition. Rats fed the diet containing 0.1% P, showed severe hypercalciuria, hypercalcemia, reduced growth and impaired bone mineralization. These effects did not occur when the diet contained 0.2 or 0.3% of P. This study suggests that in short-term studies P in the diet of female rats can be restricted to 0.2% so as to prevent nephrocalcinosis without affecting their development.
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PMID:Influence of dietary phosphorus restriction on calcium and phosphorus metabolism in rats. 252 16

Williams syndrome is characterized by peripheral artery stenosis such as supravalvular aortic stenosis, a distinctive dysmorphic facies, mental retardation and occasionally by transient infantile hypercalcemia. Twenty-five children with this syndrome underwent abdominal ultrasound examinations in our institution between 1983-1988. Five showed an increase in the renal medullary echogenicity consistent with medullary nephrocalcinosis. The echogenicity did not change with time. Two of the five had documented hypercalcemia in infancy. The other three did not have calcium measurements in infancy. No patient with normal serum calcium measurements during infancy developed nephrocalcinosis. Renal ultrasound may add information as to the incidence of infantile hypercalcemia in Williams syndrome.
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PMID:Increased renal medullary echogenicity in patients with Williams syndrome. 267 4

Severe hypercalcemia is a potentially life-threatening complication of several diseases. Most commonly it is caused by cancers that enhance bone resorption. Impaired renal calcium excretion resulting from a combination of volume contraction and calcium-induced renal injury (nephrocalcinosis) plays a critical role in the genesis and aggravation of hypercalcemia. Treatment of hypercalcemia is based on treating the underlying disease, restoring extracellular volume, correcting electrolyte deficiencies (potassium and magnesium), and reducing bone resorption. Several measures are available to reduce bone resorption, of which the most efficacious are the bisphosphonates and plicamycin (mithramycin). One of these agents in combination with volume expansion can reduce serum calcium concentrations to near normal in most patients within 3 to 6 days. Because of the delayed hypocalcemic action of these agents, they should be administered early. Calcitonin has a more modest hypocalcemic action than the bisphosphonates or plicamycin but has a more rapid effect. Combining calcitonin with plicamycin or a bisphosphonate can enhance the rate of decline of the serum calcium level. Bone resorption also can be reduced by getting patients out of bed to stand or walk. Glucocorticoids may be effective in patients with hypercalcemia associated with high levels of vitamin D, such as sarcoidosis, some lymphomas, or vitamin D intoxication. Patients with mild to moderate hypercalcemia may be asymptomatic. Therapy in these patients should be directed at the primary disease as well as at preventing complications that could raise the level of serum calcium. Efforts should be made to prevent volume contraction and prolonged bed rest. Sedatives and narcotic analgesics, by reducing activity and oral intake, can raise serum calcium levels. In the future it may be possible to predict which patients with cancer are likely to develop accelerated local tumor-mediated or humorally mediated osteolysis. For example, high circulating levels of PTH-like peptides in patients with lung cancer might suggest a greater risk of developing hypercalcemia. These patients could be monitored more closely by periodically measuring urinary calcium. Another prophylactic approach would be to treat patients at risk of developing hypercalcemia with drugs, such as the bisphosphonates, that inhibit bone resorption.
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PMID:Treatment of hypercalcemia. 267 75

Renal ultrasonography was performed on 23 patients with X-linked hypophosphatemic rickets (XLH) and 11 patients with autosomal recessive vitamin D-dependent rickets (ARVDD). A pattern of increased echogenicity of the renal pyramids (ERP) was identified in 11/23 patients with XLH and 3/11 patients with ARVDD; this ultrasonographic finding has previously been associated with medullary nephrocalcinosis. Patients with XLH and ERP had significantly higher mean serum calcium and phosphate concentrations, more frequent episodes of hypercalcemia, and higher doses of oral vitamin D and phosphate during the first 3 years of therapy. Episodes of hypercalcemia were more frequent when patients received higher doses of vitamin D2 (greater than 4000 IU/kg/day) or 1,25-dihydroxycholecalciferol (greater than 40 ng/kg/day). Episodes of hypercalciuria were significantly increased at doses of greater than 20 ng/kg/day 1,25-dihydroxycholecalciferol. In patients with ARVDD, ERP was also correlated with vitamin D dose and frequency of hypercalcemia episodes. ERP was not associated with an elevation of serum creatinine or loss of urinary concentrating ability in either patient group.
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PMID:Nephrocalcinosis and its relationship to treatment of hereditary rickets. 282 87


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