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

Powdered Cestrum diurnum leaves, mixed with two diets differing in calcium and phosphorus contents, produced nephrocalcinosis in young chicks regardless of serum calcium elevation. The calcific deposits, found in both proximal and distal portions of cortical tubules, began either in the cytoplasm or in lysosomal bodies as a unilaminar spheroid structure containing apatite crystals. The ultrastructural characteristics of intraluminal concretions suggested that they were formed intracellularly but later were extruded into the lumen. The extent of calcific deposits increased with duration and with hypercalcemia. Although Cestrum contains an analog of 1,25-dihydroxycholecalciferol, neither mitochondria nor basal lamina contained calcific deposits described in nephrocalcinosis secondary to hypervitaminosis D.
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PMID:The ultrastructure of nephrocalcinosis induced in chicks by Cestrum diurnum leaves. 746 73

Subcutaneous fat necrosis leading to hypercalcemia is rare but well documented in asphyxiated neonates. This paper presents two such neonates in whom sonography revealed the development of nephrocalcinosis and nephrolithiasis. The kidneys had initially been shown to be normal sonographically. In one infant, nephrocalcinosis developed as increasing echogenicity of the medullary pyramids. In the other, increased echogenicity of the renal cortex of uncertain cause developed together with nephrolithiasis. These sonographic appearances have not been described previously in this entity.
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PMID:Nephrocalcinosis and nephrolithiasis due to subcutaneous fat necrosis with hypercalcemia in two full-term asphyxiated neonates: sonographic findings. 759 62

We studied four children with hypercalcemia of immobilization resulting from quadriplegia. After a trial of conventional therapy, human synthetic calcitonin was given subcutaneously at 0.5 to 2.5 mg per day in divided doses. Serum calcium concentrations returned to normal levels in all patients, decreasing an average of 0.72 mmol/L (2.9 mg/dl) within 4 to 10 days. Calcitonin therapy was effective for periods varying from 3 to 10 months. In one patient a bladder stone developed without nephrocalcinosis.
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PMID:Human synthetic calcitonin therapy for hypercalcemia of immobilization. 775 17

Medullary nephrocalcinosis occurs in various diseases as a non-specific renal manifestation. We present 5 patients (hypophosphataemic rickets, type 1 renal tubular acidosis, primary hyperparathyroidism, hypercalcaemia of unclear origin, chronic renal insufficiency requiring dialysis) in whom a medullary nephrocalcinosis was demonstrated by means of sonographically detectable changes in the renal medulla region. The sonographic appearance of medullary nephrocalcinosis is characterized by detection of echo-enhanced structures in the region of the renal pyramids. The presence of a medullary nephrocalcinosis can generally be confirmed with adequate reliability on the basis of sonographic findings and characteristic clinical pictures. In individual cases it is difficult to distinguish between medullary nephrocalcinosis and renal calyx calculi.
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PMID:Medullary nephrocalcinosis: sonographic findings in adult patients. 775 19

We report a male newborn with typical clinical signs of idiopathic infantile hypercalcemia (IIH); that is, hypercalcemia, hypercalciuria, an elfin face and nephrocalcinosis without giving Vitamin D3 supplementation to the patient. He had been treated with a vitamin D-free, low calcium milk and rectal administration of exogenous calcitonin (elcatonin). The latter seemed to be more effective as a treatment for IIH. The serum calcium level came within the normal range and the serum 1,25-dihydroxyvitamin D3 (1,25[OH]2D3) level decreased from 101.5 to 75.6 pg/mL with the treatments mentioned above. These results suggest that a high serum concentration of 1,25(OH)2D3 is part of the pathogenesis of IIH. However, we were not able to clarify the pathogenesis of the high serum concentration of 1,25(OH)2D3.
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PMID:Idiopathic infantile hypercalcemia discovered in the newborn period. 787 92

This article reports the diagnostic experiences of 134 cases of primary hyperparathyroidism (PHPT) confirmed by operation and pathologic examination. The clinical presentations were divided into 4 types: (1) 75 cases (56.0%) with bone resorption; (2) 47 cases (35.0%) with bone lesions plus urinary calculus; (3) 8 cases (6.0%) with urinary calculus only and; (4) 4 cases (3.0%) with hypercalcemia only. Bone lesions included bone resorption, osteomalacia and osteoporosis. Stones at multiple sites in the urinary tract or nephrocalcinosis were found in 41 cases. The measurement of ionized calcium was much more sensitive and accurate than the total calcium assay with the positive rate of 95.3% and 73.4% respectively. The concentration of plasma iPTH was high in the whole group (n = 84), the mean value was 21.4 +/- 17.9 times higher than that of the normal control group. For the localization of the affected parathyroid gland, instiat examination was by neck ultrasonography which gone a positive predictive value of 81.5% (43/53), 99mTc-MIBI scan showed positive rate 94.1% (16/17). The CT scan of the chest was used when ectopic location in mediastinum was highly suspected. If the first operative exploration failed to find the affected parathyroid gland, we performed the determinations of iPTH with samples taken from internal jugular vein through selective venous catheterization; the coincidence rate was found to be 85.2% (23/27).
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PMID:[The diagnosis of primary hyperparathyroidism--analysis of 134 cases]. 795 61

Vitamin D and its metabolites are well-established regulators of bone mineral homeostasis. Their clearest role is in the prevention and treatment of rickets and osteomalacia, bone diseases characterized by inadequate bone formation, and mineralization. Much of the effectiveness of vitamin D and its active metabolite 1,25(OH)2D in treating such disorders rests with their ability to increase serum levels of calcium and phosphate principally by stimulating intestinal calcium and phosphate absorption. Osteoporosis is not a disease resulting from obvious deficiencies in vitamin D, calcium, and phosphate. More subtle deficiencies, however, may be found, especially among the elderly with decreased intake of dairy products, reduced sunlight exposure, and less efficient intestinal absorption of bone minerals. Such subtle deficiencies may account for the ability of vitamin D and calcium supplementation to have a beneficial effect on bone mineral density in this population. Estrogen administration to postmenopausal females raises 1,25(OH)2D levels, presumably through increased renal production, and this increase is associated with increased intestinal calcium transport. Serum measurements of the vitamin D metabolites in general, however, and 1,25(OH)2D in particular do not consistently show evidence of a decrease at the time of menopause. Although most studies show a fall in intestinal calcium transport with age, which can be reversed with 1,25(OH)2D or estrogen, even these observations have not been found consistently. Thus, some investigators have addressed the issue of tissue resistance to 1,25(OH)2D and have noted decreased VDR in the intestine and reduced 1,25(OH)2D accumulation by bone with age. Despite no obvious deficiency of vitamin D in most patients with osteoporosis, clinical trials with vitamin D or 1,25(OH)2D show promise. Vitamin D treatment will probably prove most efficacious in populations with marginal vitamin D intake and/or limited sunlight exposure; high doses would not be required, and the treatment would be safe. This would be a physiologic and not a pharmacologic use of vitamin D. The use of 1,25(OH)2D for treatment of osteoporosis in individuals with adequate nutrition and sunlight exposure may require somewhat higher than physiologic doses to be effective. Perhaps such doses are necessary to stimulate osteoblast activity and/or differentiation; by raising the serum calcium level, such doses of 1,25(OH)2D might block its otherwise stimulatory effect on osteoclast number and activity. Such doses run the risk of hypercalcemia and hypercalciuria, leading to nephrolithiasis and/or nephrocalcinosis. These undesirable side effects appear to be less common with the use of 1 alpha OHD compared with 1,25(OH)2D, but this may be because of the lower levels of calcium consumption in Japan where 1 alpha OHD is widely prescribed.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Role of vitamin D, its metabolites, and analogs in the management of osteoporosis. 798 88

X-linked hypophosphatemia, currently one of the most prevalent varieties of familiar rickets, is attributed to renal phosphate wasting secondary to a gene defect localized to X p22 chromosomal region. The proximal tubular phosphate reabsorption defect is associated with blunted 1,25-dihydroxyvitamin D synthesis to hypophosphatemia or parathyroid hormone administration. It is characterized clinically by hypophosphatemia, growth retardation, and rickets especially in male patients. As the affected patients mature, pseudofractures, skeletal deformities, osteomalacic bone pain, progressive ankylosis, and dental caries occur, which may be alleviated and even prevented with adequate medical therapy. Long term treatment combines phosphate supplementation with calcitriol, augmented occasionally by diuretics. Hypercalcemia, hyperparathyroidism, and nephrocalcinosis are potential complications which require careful monitoring and continued investigations. The use of recombinant human growth hormone to augment renal tubular reabsorption of phosphate and to promote linear growth remains to be examined in well controlled, clinical trials.
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PMID:X-linked hypophosphatemia: molecular biology and treatment controversies. 804

The treatment of X-linked hypophosphatemia (XLH) consists of phosphate and vitamin D3 derivatives. Transient hypercalciuria and hypercalcemia are well-known signs of vitamin D intoxication. Despite urinary calcium excretion control, the danger of nephrocalcinosis in treated patients has been emphasized. It has recently been suggested that hyperoxaluria might be a causative factor of nephrocalcinosis other than calcium in phosphate-treated XLH patients. We measured urinary oxalate and phosphate excretion in 12 patients with the syndrome of hereditary hypophosphatemic rickets with hypercalciuria (HHRH) receiving only oral phosphates and in 5 XLH patients receiving both oral phosphates and vitamin D. No correlation was found between the dosage of phosphate supplements or urinary phosphate excretion and urinary oxalate excretion, in either group of patients. Nephrocalcinosis, presenting as hyperechogenicity of the medullary pyramids, was found in 2 of the 5 XLH patients and only in 2 HHRH patients who had been treated with excessive doses of vitamin D2 and calcium, prior to the true diagnosis being established. We conclude: (1) hyperoxaluria is not a cause of nephrocalcinosis in phosphate-treated patients with hereditary hypophosphatemic rickets; (2) prolonged phosphate treatment alone does not induce nephrocalcinosis in HHRH patients, and (3) we believe that in XLH patients, nephrocalcinosis is essentially due to vitamin D overdosage at some stage, or noncompliance in phosphate intake, leading to repeated undetected hypercalciuric periods.
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PMID:Hyperoxaluria is not a cause of nephrocalcinosis in phosphate-treated patients with hereditary hypophosphatemic rickets. 839 9

Primary hyperparathyroidism in childhood is rare. Long-standing hypercalcaemia is reported to result in severe and irreversible renal damage. However, renal complications of hyperparathyroidism, particularly nephrocalcinosis are uncommon. We report a 12-year-old girl presenting after three years with extensive nephrocalcinosis and with rapid recovery of renal function.
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PMID:Renal function in hyperparathyroidism with complicating nephrocalcinosis. 845 6


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