Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020437 (hypercalcemia)
 10,293 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A middle-aged farmer and a female student presented with osteitis fibrosa cystica with nephrocalcinosis in the former and nephrolithiasis in the latter due to primary hyperparathyroidism. Hypercalcaemia was present in both cases and neck exploration revealed a large solitary parathyroid adenoma which was excised. Because primary hyperparathyroidism is less common in tropical countries doctors may be less familiar with the early manifestations of the disease. The number of patients thus undiagnosed and untreated is unknown.
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PMID:Parathyroid adenoma in northern Nigeria. 847 Mar 6

We tabulated the frequency of renal abnormalities in 40 Williams syndrome individuals presenting for medical and/or developmental assessment to a multi-disciplinary Williams syndrome program. The average age at time of assessment was 7 2/12 years. Seven individuals (7/40 = 18%) had abnormalities detected, including nephrocalcinosis = 2; marked asymmetry in kidney size = 2; small kidneys = 1; solitary kidney = 1; and pelvic kidney = 1. Renal function was also assessed. Two individuals had evidence of renal dysfunction, one secondary to nephrocalcinosis and the second due to hypercalcemia and interstitial nephritis of unclear pathogenesis. We examined the frequency of renal artery stenosis in 9 individuals who underwent abdominal angiography during cardiac catheterization. We found unilateral or bilateral mild renal artery narrowing in 4 individuals and normal renal arteries in the remaining 5. Persistent hypertension occurred in only 2 individuals and did not correlate with renal artery status. We conclude that intrinsic renal anomalies, as well as problems secondary to hypercalcemia, occur with sufficient frequency to warrant baseline renal screening in all individuals with Williams syndrome.
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PMID:Renal findings in 40 individuals with Williams syndrome. 848 70

Sarcoidosis has been associated with a wide spectrum of renal manifestations, including disordered calcium metabolism, nephrocalcinosis, nephrolithiasis, granulomatous interstitial nephritis, and glomerulonephritis. In some patients, two or more manifestations of renal sarcoidosis may coexist. The case of a young patient with sarcoidosis who presented with hypercalcemia and acute renal failure is discussed. Despite normalization of the serum calcium with intravenous fluids and corticosteroids, his renal insufficiency persisted. A diagnostic renal biopsy was performed to determine the etiology of his renal failure and was helpful in the selection of optimal medical therapy.
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PMID:The kidney in sarcoidosis. 850 10

We describe 11 infants with congenital lactase deficiency, whose age at diagnosis varied from 6 to 88 days. At the time of admission, 7 of 10 infants had hypercalcemia. Five of the seven infants for whom renal ultrasonography was performed at the time of diagnosis had medullary nephrocalcinosis. Hypercalcemia ceased within a week of the start of a lactose-free diet. At the time of reevaluation, at the ages of 2 to 10 years, one of the patients still had hypercalciuria and nephrocalcinosis was still present in 3 of 11 patients. The mechanism of hypercalcemia is unclear but may be related to metabolic acidosis or may be promoted by the lactose effect (i.e., by nonhydrolyzed lactose that has a direct enhancing effect on calcium absorption in the ileum).
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PMID:Hypercalcemia and nephrocalcinosis in patients with congenital lactase deficiency. 852 89

Biological responses mediated by vitamin D occur as a consequence of the integrated actions of the vitamin D endocrine system. The vitamin D endocrine system is characterized by the sequential two-step metabolism of vitamin D to 1 alpha,25(OH)2D3 by the liver and kidney, and by the ability to generate biological responses in over 30 target tissues through nuclear receptor (nVDR) regulation of gene transcription and nongenomic pathways. It is now clear that the vitamin D endocrine system embraces many more target tissues than simply the intestine, bone and kidney. Notable additions to this list of tissues containing the nVDR include pancreatic B cells, pituitary gland, breast tissue, placenta, lymphocytes, keratinocytes, colon, and prostate, as well as many cancer cell lines. In addition to the classical actions of 1 alpha,25(OH)2D3 on mediating calcium homeostasis, this seco steroid has been identified as a potent stimulator of cell differentiation as well as an inhibitor of proliferation. Over the past decade at least 400 analogs of 1 alpha,25(OH)2D3 have been chemically synthesized and their biological properties systematically explored in a variety of assays which quantified both their calcemic effects and cell differentiating potential. The objective has been to identify new analogs devoid of the classical calcemic consequences of high doses of 1 alpha,25(OH)2D3, namely hypercalcemia, soft tissue calcification and nephrocalcinosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The vitamin D Endocrine system: manipulation of structure-function relationships to provide opportunities for development of new cancer chemopreventive and immunosuppressive agents. 853 1

The causes of the development of nephrocalcinosis in familial hypophosphatemic rickets (FHR) are reviewed. The treatment combines vitamin D or 1,25 dihydroxyvitamin D and oral phosphate supplementation. Hypercalcaemia and hypercalciuria were thought to cause the renal calcification. On the basis of the data of eighteen patients with familiar hypophosphatemic rickets we have found that the main difference between the treatment of patients having nephrocalcinosis and those with normal renal morphology consisted in the dose of oral phosphate intake. Patients with nephrocalcinosis received significantly higher doses of oral phosphate (130 mg/kg/day versus 70 mg/kg/day, p < 0.01). Correspondingly, their urinary phosphate excretion was also significantly higher (p < 0.01). There was no difference between the two groups with respect of the doses of vitamin D and urinary calcium excretion. It can be concluded, that high concentrations of urinary phosphate can lead to nephrocalcinosis even if urinary calcium concentration is normal. In order to prevent nephrocalcinosis in patients with X-linked hypophosphatemia, the following guide-lines could be recommended: 1) urinary calcium excretion should be kept lower, than the usually allowed < 4 mg/kg/day; 2) oral phosphate supplementation should not exceed 100 mg/kg/day, 3) patients should be encouraged to drink large amounts of water, 4) regular ultrasound controls should be part of the routine follow-up.
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PMID:Guide-lines to the treatment of patients with X-linked hypophosphatemic rickets. 857 31

We present the case of an adolescent with hypercalcemia secondary to unrecognized hyperparathyroidism, which lead to complications such as pancreatitis, diabetes mellitus, and nephrocalcinosis. Although hypercalcemia is not common in the pediatric age, its early recognition and intervention are crucial for the prevention of highly morbid complications.
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PMID:Primary hyperparathyroidism: an unusual cause of pancreatitis in adolescence. 858 19

The introduction of renal ultrasound technology has shown renal calcification to be more common in infancy than was previously believed. Understanding the role of inhibitors and promoters in crystal formation helps elucidate the pathophysiology of nephrocalcinosis. Identification of the presence or absence of hypercalcemia and hypercalciuria is an effective way to direct the diagnostic work-up of infants with nephrocalcinosis. The sonographic image of renal calcification resolves spontaneously in many infants. Whether microscopic nephrocalcinosis persists below the threshold of ultrasonographic detection is unknown. Renal calcification can be associated with persistent renal function abnormalities if hypercalciuria continues, such as in VLBW infants who receive long-term furosemide therapy after discharge from the hospital. Renal calcification may also progress to renal failure, such as in infants with primary hyperoxaluria, owing to the persistence of hyperoxaluria, a potent promoter of calcium crystal formation.
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PMID:Renal calcification in the first year of life. 861 92

Hypercalcemia occurs in about 10% of the patients with sarcoidosis; hypercalciuria is about three times more frequent. These abnormalities of calcium metabolism are due to dysregulated production of 1,25-(OH)2-D3 (calcitriol) by activated macrophages trapped in pulmonary alveoli and granulomatous inflammation. Undetected hypercalcemia and hypercalciuria can cause nephrocalcinosis, renal stones, and renal failure. Corticosteroids cause prompt reversal of the metabolic defect. Chloroquine, hydroxychloroqune, and ketoconazole are the drugs that should be used if the patient fails to respond or develops dangerous side effects to corticosteroid therapy.
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PMID:Vitamin D, calcium, and sarcoidosis. 862 Jul 32

Hypercalcaemia is one of the extra-pulmonary symptoms of sarcoidosis. We describe a case of acute and chronic renal failure due to urolithiasis and nephrocalcinosis probably caused by sunlight-induced hypercalcaemia in a patient with undiagnosed sarcoidosis. Attention must be given to excessive sun exposure and vitamin D intake in patients with sarcoidosis.
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PMID:[Nephrocalcinosis and urolithiasis as primary symptoms in Boeck's sarcoidosis]. 864 14


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