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

A 52 year old man with a long history of marked hypertension, peptic ulcer disease, nephrocalcinosis and intermittent hypercalcemia was referred to be evaluated for primary aldosteronism suspected on the basis of low plasma renin activity, hypokalemia and blood pressure responsive to spironolactone. Aldosterone excretion, however, was extremely low. Alkaluria, high urinary sodium excretion and hypercalciuria were observed. The patient admitted to chronic ingestion of large amounts of baking soda. Upon cessation of alkali abuse, his blood pressure fell dramatically; orthostatic hypotension, concomitant azotemia, hemoconcentration, hyperkalemia and weight loss occurred. Despite dramatic elevation in plasma renin activity, urinary aldosterone excretion remained low during this period. Adrenal glucocorticoid secretion was intact. All abnormalities of sodium, potassium and aldosterone subsequently returned to normal. A 10 day challenge with oral sodium bicarbonate was associated with a rise in blood pressure, but serum calcium remained normal. The patient remains normotensive 15 months after discontinuing alkali abuse.
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PMID:Hypertension corrected by discontinuing chronic sodium bicarbonate ingestion. Subsequent transient hypoaldosteronism. 111 72

The development of nephrocalcinosis in the rat following intraperitoneal injections of various concentrations of neutral sodium phosphate (pH 7-4) was studied using histology, histochemistry, electron microscopy and quantitative techniques. Daily injections of 0-5 M phosphate consistently produced nephrocalcinosis after 6 days or more. Calcium deposits were at first confined to the basement membranes of proximal tubules; but a longer course of injections, up to 10 days, resulted in additional basement membrane calcification in the outer cortes, and outer medulla, together with intra-luminal casts, often calcified, in the outer medulla and papilla. Calcification was not found in other organs such as liver, lung, heart or aorta. Results from quantitative estimations of total kidney calcium and phosphorus suggested that it was the calcium content which was important to the initiation of nephrocalcinosis. Ultrastructural changes, suggestive of degeneration or alteration in function, were found in mitochondria of proximal tubules in experimental animals before the onset of histologically evident nephrocalcinosis. Later changes, especially to the basal part of proximal tubular cells and their basal laminae, were thought to be consequent upon the mitochondrial changes. It is suggested that the initial renal damage was caused both directly, by a toxic effect of the phosphate load on the kidney and, indirectly, by stimulation of the parathyroid glands as a result of the hypocalcaemia and hyperphosphataemia which followed an injection of phosphate. Daily doses of 1 M phosphate for 3 days produced a type of nephrocalcinosis which was more typical of that reported by previous investigators, who used high doses of phosphate. Twice daily injections of 0-25 M phosphate for 6 days did not induce nephrocalcinosis, whereas 0-375 M phosphate given twice daily for 6 days produced only minimal calcium deposits compared with animals given 0-5 M phosphate once daily for the same period. This may have important clinical implications, since phosphate has been used to control hypercalcaemia of various etiologies.
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PMID:The development of nephrocalcinosis in the rat following injections of neutral sodium phosphate. 113 87

The autopsy findings of two cases of infantile hypophosphatasia are described and compared with those of 16 previously reported cases. Histochemical and biochemical tissue analysis for alkaline phosphatase showed a marked decrease in activity in liver, kidney, and bones. However, intestinal alkaline phosphatase possessed normal or slightly elevated activity. Nephrocalcinosis is a frequent complication and its development depends on hypercalcemia and length of survival of the patient. Electron microscopic findings are illustrated, and a mechanism for the development of nephrocalcinosis is proposed. For the first time, marked elevations of parathyroid hormone was detected. This finding, coupled with the extreme difficulty in locating the parathyroid glands in cases of hypophosphatasia, is enigmatic. Areas for furture investigation are suggested.
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PMID:Hypophosphatasia-study on two autopsy cases. 119 30

Anorexia, severe skeletal demineralization, and muscular weaknesss developed in a 9 year-old Collie. Hypercalcemia, hypophosphatemia, and nephrocalcinosis were found on clinical evaluation. The surgical removal of a parathyroid adenoma was followed by profound hypocalcemia that was unresponsive to calcium therapy, and the dog died. The persistent hypocalcemia was attributed to increased deposition of calcium in mineral-deficient bone.
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PMID:Primary hyperparathyroidism in a dog. 126 47

The established prophylaxis for vitamin D-deficient rickets today is 400 IU vitamin D3 given daily during the first year of life. With this regimen, vitamin D intoxication is a rare event. Nevertheless, we have recently seen 4 infants with vitamin D intoxication after a so called "stoss" prophylaxis, i.e. twice 300,000 units (7.5 mg) vitamin D3 orally within 4 weeks. One patient presented with failure to thrive due to marked hypercalcemia (3.9 mmol/l) and nephrocalcinosis, 2 patients showed medullary nephrocalcinosis on ultrasonography and one patient had gross hematuria and spontaneous passage of a calculus. Three patients had massive hypercalciuria (calcium/creatinine ratio 1.8-4.8 mol/mol, normal less than 1). The 25 (OH) vitamin D3 plasma levels, measured only in 2 patients, were strikingly increased (270 and 158 nmol/l, respectively, normal 25-80). Urinary calcium excretion slowly decreased to normal values on a low calcium diet and high fluid intake. Nephrocalcinosis, however, persisted in 2 patients and showed a slight progression ultrasonographically in one patient. The short time interval between vitamin D administration and onset of symptoms and the subsequent clinical course provide strong evidence that hypercalciuria and nephrocalcinosis were due to vitamin D "stoss" prophylaxis in all four cases. In conclusion, there is no indication for vitamin D "stoss" prophylaxis for vitamin D-deficient rickets in infants. Vitamin D intoxication still has to be considered as a possible cause of hypercalciuria.
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PMID:[Vitamin D poisoning in infants: a preventable cause of hypercalciuria and nephrocalcinosis]. 131 65

Nephrocalcinosis is uncommon in childhood, the main causes are renal tubular acidosis, hyperparathyroidism and medullary sponge kidney. It is also seen where there is hypercalcaemia or hypercalciuria of any aetiology; We report nephrocalcinosis in an 18-month-old infant with metaphyseal chondrodysplasia type Jansen and also in a neonate with McCune Albright syndrome who displayed atypical skeletal appearances and had multiple ovarian cysts.
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PMID:Two unusual cases of nephrocalcinosis in infancy. 143 81

Three patients with nonpulmonary sarcoidosis had chronic erythema nodosum within the first 2 years of life. Each subsequently had renal sarcoidosis and nephrocalcinosis; hypercalcemia was documented in each patient and hypercalciuria in two patients. Treatment with prednisone was not uniformly successful in normalizing creatinine clearance. Nephrocalcinosis may be more common than previously reported in patients with sarcoidosis.
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PMID:Sarcoidosis associated with nephrocalcinosis in young children. 144 62

A sixty nine-year-old woman was admitted to the hospital because of further examination of hypercalcemia. On July 1990, she complained of general fatigue and loss of appetite. She was pointed out to have hypercalcemia (15.1mg/dl), urolithiasis, and renal insufficiency. CT films of the chest showed swelling of the mediastinal lymphnodes and CT of the abdomen nephrocalcinosis. Ga-scintigraphy demonstrated an abnormal accumulation of gallium in the mediastinum. Levels of the parathyroid hormone was normal. Levels of the serum calcium (13.7mg/dl), angiotensin converting enzyme (30.4IU/L) and 1.25 (OH)2D (87PG/ml) were elevated. Giant cells were found in the biopsy specimen of the lung. A significant relationship between the serum calcium and creatinine were observed (r = 0.76, p < 0.02). Proximal fractional reabsorption of sodium showed to be suppressed (47.7%), and distal fractional reabsorption of sodium showed to be normal (88.4%). From these findings hypercalcemia and urolithiasis was suggested to result from sarcoidosis. The hypercalcemia and renal insufficiency improved with corticosteroid therapy.
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PMID:[A case of sarcoidosis with hypercalcemia, urolithiasis, nephrocalcinosis and renal insufficiency]. 148 16

We report on a 7-week-old infant with idiopathic hypercalcemia, hypercalciuria and nephrocalcinosis. At the time of admission, serum concentrations of parathyroid hormone and 1,25(OH)2D3 were found to be inadequately high, and those of calcitonin and 24,25(OH)2D3 too low, relative to the hypercalcemia. Treatment with calcitonin normalized serum calcium concentrations within 4 days, and a 3-week course of thiazides combined with a decreased dietary calcium:phosphorus ratio corrected the hypercalciuria. A repeat profile of the calcium-regulating hormones done at the age of 5.5 months was normal. Based on the clinical course and the hormonal profiles, we hypothesize that the idiopathic infantile hypercalcemia in this patient could have resulted from a generalized maturational delay of calcium homeostasis. Treatment with calcitonin, therefore, seems to be the most appropriate way to control the hypercalcemia.
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PMID:Idiopathic infantile hypercalcemia: rapid response to treatment with calcitonin. 160 83

A patient with hypophosphatemic vitamin D-resistant rickets developed secondary erythrocytosis during treatment with large doses of vitamin D2 and phosphate. Erythrocytosis was accompanied by a fall in circulating plasma volume and appeared to have developed as a consequence of nephrocalcinosis because it occurred after the appearance of nephrocalcinosis following several episodes of hypercalcemia and hyperphosphatemia. Nephrocalcinosis and erythrocytosis did not disappear even after recovery of renal function. Thus, the present observations point to the importance of preventing these irreversible complications that could cause renal failure, erythrocytosis, and thrombotic events during the management of hypophosphatemic vitamin D-resistant rickets.
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PMID:Erythrocytosis in hypophosphatemic rickets: irreversible complication due to nephrocalcinosis after vitamin D and phosphate therapy. 166 79


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