Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020438 (hypercalciuria)
 2,502 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

We describe a patient who initially formed calcium-containing renal stones owing to gouty diathesis and hypocitraturia. On therapy with 300 mg. allopurinol and 60 mEq. potassium citrate daily serum uric acid decreased from 9.2 to 5.8 mg. per dl., urinary pH increased from less than 5.5 to 6.6 and urinary citrate increased from 223 to 1,005 mg. per day. Four months later while still on this medical regimen, the patient presented with hypercalcemia (13.4 mg. per dl.), high serum 1,25-dihydroxyvitamin D (65 pg. per ml.) and hypercalciuria (598 mg. per day), which subsequently were found to result from sarcoidosis. Prednisone therapy normalized the disturbances in calcium metabolism. During 33 months of combined treatment with 7.5 to 10 mg. prednisone a day, allopurinol and potassium citrate, the patient was free of stones and he had normal urinary calcium, pH and citrate. However, a calcium stone formed 1 month after discontinuation of prednisone therapy, although treatment with allopurinol and potassium citrate was continued. The patient had marked hypercalciuria of 447 to 465 mg. per day, despite normal urinary pH, citrate and uric acid. This case represents calcium stone formation in a patient with 2 separate etiologies for stone disease, that is gouty diathesis and sarcoidosis. Therapeutic regimens directed at the correction of both metabolic disturbances were required to control renal stone formation.
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PMID:Gouty diathesis and sarcoidosis in patient with recurrent calcium nephrolithiasis. 337 3

Although hypercalcemia has long been recognized as a complication of sarcoidosis, the incidence of hypercalcemia (> or = 11 mg/dl) in Japan is probably less than 5%. 1 alpha, 25(OH)2D3 is the main cause for hypercalcemia in sarcoidosis and overproduced by sarcoid granulomata. Gamma-interferon produced by activated lymphocytes and macrophages plays a major role in the synthesis of 1 alpha, 25(OH)2D3. PTH release is down regulated by high serum concentration of 1 alpha, 25(OH)2D3. Parathyroid hormone related protein may also contribute to the hypercalcemia of sarcoidosis. Treatment of hypercalcemia and hypercalciuria consists of a low calcium diet, adequate hydration, minimization of exposure to sunlight and reducing overproduction of 1 alpha, 25(OH)2D3. Prednisone, 15 to 25 mg/day, is the drug of choice to reduce the overproduction of 1 alpha, 25(OH)2D3.
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PMID:[Hypercalcemia in sarcoidosis]. 1223 75