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

Ten children with Bartter's syndrome are described. Their ages at diagnosis ranged from three months to 15 years and there was an equal sex distribution. A wide spectrum of severity of clinical and biochemical features was found. Hypercalcaemia, hypophosphataemia, hypercalcuria, nephrocalcinosis, rickets and urine acidification defects were seen in some patients. Two affected children were siblings. Six children were treated over periods of six to 24 months with indomethacin with remarkable clinical and biochemical improvement. Catch-up growth was demonstrated in all treated cases. Tolerance to indomethacin appeared to develop in some children. Only one serious complication was seen with this therapy, a duodenal ulcer in a child on high dosage. Of those children not treated with indomethacin, one died, one is now on indomethacin elsewhere and two are well without therapy.
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PMID:Bartter's syndrome: 10 cases in childhood. Results of long-term indomethacin therapy. 12 May 50

Acute massive vitamin D overdosage occurred in a family after eating food cooked in a nut oil containing 5 million units of vitamin D3/ml. The plasma vitamin D was 55 and 60 i.u./ml in the father and mother respectively, and 9.6 i.u./ml in their 11-month-old infant (normal range, 0--1.6 i.u/ml). All the family presented with symptoms of hypercalcaemia and the infant responded quickly to prednisone. After steroids had failed to control the hypercalcaemia in the parents, neutral phosphate was successful, although necessary for 9 months. Before phosphate therapy it was shown that both parents were in strongly negative calcium balance, indicating that the vitamin D was mobilizing calcium from bone. Eleven years later all 3 patients are well but a renal biopsy in one of them shows persistent nephrocalcinosis.
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PMID:A family with massive acute vitamin D intoxication. 23 12

Fifteen cases of hypervitaminosis D in childhood are reviewed. In all of them, vitamin D was given following medical prescription. In four occasions, excessive dosage of vitamine D impaired the evolution of a previous nephropathy. The clinical, analytical, radiological and histological findings as well as the therapeutical aspects are commented. Hypercalcemia, hypercalciuria, polyuria with hypostenuria, renal failure, bone lesions and nephrocalcinosis are the most prominent features of the picture. Occasionally, arterial hypertension and glycosuria were found. Prednisone, thyrocalcitonine and phosphates were used as therapeutical means. In spite of nephrocalcinosis and renal failure generally present at diagnosis, the clinical course was rather good.
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PMID:[Hypervitaminosis D. Review of fifteen cases]. 44 41

A case of idiopathic hypercalcaemia diagnosed in a six months old infant is reported. Nephrologic symptoms were conspicuous: decreased clearance, increased serum creatinin and urea nitrogen level, restricted ability of concentration, damage of the renal acidification; slight nephrocalcinosis was shown histologically. The serum calcium level and calcium excretion became normal under the treatment with hydrochlorothiazide and prednisolon. The function of the kidney and the general status of the infant significantly improved.
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PMID:[Idiopathic hypercalcaemia. The effect of hypercalcaemia on renal function (author's transl)]. 49 89

Six patients with biopsy-proven renal sarcoidosis presented with renal failure of unknown origin; in none was the diagnosis of sarcoidosis initially considered. The serum creatinine concentration at the time of presentation ranged from 265 to 1380 mumol/l (3.0 to 15.6 mg/dl), with a mean of 787 mumol/l (8.9 mg/dl). Although only two patients were hypercalcemic at the time of presentation, the 24-hour urinary excretion of calcium was increased in three of the four patients in whom it was measured, and renal calculi were present in one case. Renal biopsy revealed interstitial nephritis and tubular atrophy in all cases, as well as nephrocalcinosis in three cases and noncaseating granulomas negative for acid-fast bacilli in four cases. In each patient steroid therapy led to a rapid improvement in renal function (mean post-treatment serum creatinine level 274 mumol/l [3.1 mg/dl]). The follow-up period ranged from 8 months to 8 years (mean 3.0 years). In three patients renal function remained stable with low-dose steroid therapy. In two cases recurrent hypercalcemia and deteriorating renal function accompanied steroid withdrawal but resolved with its reinstitution. In one additional case reversible deterioration in renal function accompanied tapering of the steroid dose; however, there was no hypercalcemia.This report emphasizes the importance of considering sarcoidosis in the differential diagnosis of acute renal failure of unknown origin. Long-term follow-up of such patients is essential, as relapse is common.
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PMID:Clinical and pathological features of six cases of sarcoidosis presenting with renal failure. 51 62

On the basis of 100 cases of hypercalcemia, the authors attempt to elucidate the criteria of the etiologic diagnosis. Kidney lithiasis or nephrocalcinosis suggested a primary hyperparathyroidism (HPT I) or an intoxication due to vitamin D. X rays of the skeleton and quantitative histological exams of the bone were not useful in the diagnosis of HPT I. The level of parathormone in the plasma is the best parameter to be used in distinguishing HPT I from other diseases. In the absence of renal insufficiency or severe intestinal disorders, a phospharemia below 2.6 mg/100 ml, a chloremia above 103 m EG/l and bicarbonates below 25 m Eg/l indicate an HPT I or a paraneoplasic. A phosphoremia above 3.2 mg/100 ml runs counter to this diagnosis. The chloremia/phosphoremia ratio is not more helpful than the phosphoremia alone.
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PMID:[Etiologic diagnosis of hypercalcemia. A study of 100 cases]. 72 66

Nine of ninety patients with sarcoidosis were found to have significant renal impairment. Epithelioid granulomata were present in five of eight patients who had renal biopsies and glomerular lesions were present in six. There was close correlation between hypercalcaemia, hyperuricaemia, nephrocalcinosis and creatinine clearance. In one patient, renal sarcoidosis complicated membrano-proliferative glomerulonephritis and one patient died in end-stage renal disease.
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PMID:Sarcoidosis with renal involvement. 73 83

Four patients having high-level quadriplegia developed elevated serum calcium concentrations (11 to 15.8 mg/100 ml) within three months of injury. All were young males (ages 15 to 19 years) and quadriplegic (C4-C7). Presenting symptoms were nausea, vomiting, polydipsia, polyuria and lethargy. In two patients severe muscle wasting and cachexia with clinical symptoms developed and persisted for several months. Laboratory studies in all patients showed negative calcium balance with hypercalciuria. Reduced renal function was seen in all patients but returned to normal with return of normal serum calcium. Alkaline phosphatase level was normal in three and elevated in one. Serum parathormone levels were normal. Roentgenograms revealed diffuse demineralization. Nephrocalcinosis and soft tissue calcifications developed in one patient. Primary treatment included reduced calcium intake, correction of dehydration, sodium infusion and remobilization. Corticosteroids, oral phosphates, furosemide and mithramycin were used with varying success to control prologned symptoms and severe hypercalcemia.
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PMID:Immobilization hypercalcemia in spinal cord injury. 83 59

A 60-year-old man with a history of excessive ingestion of calcium carbonate presented with azotemia, hypercalcemia and hyperphosphatemia. His acid-base status was initially normal. Following the cessation of calcium carbonate treatment, the hypercalcemia and azotemia disappeared, and the patient was found to be in metabolic acidosis with blunted acid excretion and a urine pH of 6.1. Kidney biopsy showed focal tubular calcification; the tubular damage was apparently caused by hypercalcemia and had resulted in renal tubular acidosis. During the three months of observation since that time there has been a tendecy for spontaneous remission of the renal tubular acidosis. Impaired renal hydrogen ion excretion prevented the development of metabolic alkalosis despite ingestion of alkali initially, and was later responsible for the metabolic acidosis. Renal tubular acidosis occurring as a sequel to the milk-alkali syndrome may aggravate the danger of nephrocalcinosis in this syndrome.
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PMID:Renal tubular acidosis due to the milk-alkali syndrome. 88 14

The diangosis, clinical manifestations and management of 11 children with nephrocalcinosis encountered in a 20-year period are presented. Renal tubular acidosis, primary hyperoxaluria, primary hyperparathyroidism, exogenous hyperadrenocorticism and idiopathic hypercalcemia of infancy were the principal causes of nephrocalcinosis in this series. In the presence of normal or near-normal renal function, a 55 per cent or better cure rate can be expected. Children with significantly diminished renal function have a poor prognosis and should be considered for renal transplantation.
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PMID:Nephrocalcinosis in infancy and childhood. 109 88


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