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

Light microscopic examination of kidney tissue of guinea pigs exposed to 1.5% CO2, 21% O2, and balance N2 for periods as long as 42 days and of rats exposed to the same CO2 concentrations for up to 91 days showed that the incidence of focal kidney calcification increased with length of exposure. Calcification occurred primarily in the tubules of the renal cortex. Another group of guinea pigs were exposed to 1% CO2, 21% O2, and the balance N2 for periods up to six weeks and were later killed at regular intervals, together with control animals of the same litter. In the exposed animals, arterial PCO2 was elevated by 3-4 mmHg and hydrogen ions by about 4 nmol/liter. The standard bicarbonate level was lowered by 1-1.5 mmol, indicating a lack of renal reabsorption of bicarbonate (HCO3), which in turn placed greater stress on the bone buffer system and apparently caused bone calcium and phosphorus mobilization. Bone calcium and phosphorus levels exhibited a cyclic decrease, which resulted in cyclic hypercalcemia and hyperphosphatemia, after one week and six weeks of exposure to 1% CO2. Kidney calcium content increased significantly after two weeks of exposure (27%) and remained at this elevated level during subsequent exposures between the third and sixth weeks. These findings indicate that once the kidney calcification process has started, kidney mineralization is independent of fluctuations in the blood calcium level. A rise in plasma phosphate level that occurred after one day of exposure could have been a precipitating factor in the calcification process. The small but consistent increases in ionized calcium during a 4-week exposure to 1% CO2 may have stimulated the parathyroid, causing an increased blood calcium level that was independent of the two calcium tides in the blood associated with marked bone calcium loss.
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PMID:CO2-induced kidney calcification. 4 51

Two patients with Burkitt's lymphoma presented with severe hypercalcemia, a previously unreported complication of this tumor. Roentgenograms and radionuclide scans showed multiple osteolytic lesions in both patients. Plasma parathyroid hormone (PTH) was undetectable during the hypercalcemia phase. Chemotherapy was followed by rapid tumor lysis, hyperphosphatemia, phosphaturia and hypocalcemia. The hypocalcemic phase persisted for two weeks despite rapid normalization of serum phosphorus and renal function. Measurement of urinary cyclic AMP, an index of PTH action, indicated that parathyroid function had been suppressed by the hypercalcemia and remained suppressed for almost one week despite marked hypocalcemia.
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PMID:Hypercalcemia with suppressed parathyroid hormone in Burkitt's lymphoma. 20 38

Single administration of 0.25 microgram of sunthetic Ialpha-hydroxycholecalciferol (IalphaOHD3) into nephrectomized rats, maintained at D-avitaminous diet, improved the active transport of calcium ions against the concentration gradient in small intestine of these animals, whereas ergocalciferol was biologically inactive under the same conditions. Administration of IalphaOHD3 during 5 days at a dose 0.025 microgram normalized calcium content in blood serum of rats with D-avitaminosis, Increased doses of IalphaOHD3, administered into intact animals, caused transient hyperphosphatemia, hypercalcemia, calcinosis of internal tissues (kidney heart, aorta) as well as death of some animals. IalphaOHD3 exceeded 400-fold the hypercalcemic and calcinose effects of ergocalciferol. LD50 for IalphaOHD3 was equal to 100 microgram/kg, if it was administered during 5 days per os. Tissue calcinosis was developed after administration of a daily dose 10 microgram/kg, moderate hypercalcemia was caused by a daily dose 1 microgram/kg or 0.25 microgram per an animal; this amount is only 10-fold higher as compared with the physiologic requirement. Ergocalciferol caused hypercalcemia and metastatic calcification only at a dose 4000 microgram/kg. Clinical use of IalphaOHD3 at doses, exceeding the physiologic requirements, has to be prohibited due to high activity of the preparation and to toxicity of its increased doses.
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PMID:[Comparative study of the biological activity and toxic effect of 1alpha-hydroxycholecalciferol and ergocalciferol in rats]. 30 16

The prophylaxis and treatment of renal osteodystrophy are based on pathophysiological principles. Development of secondary hyperparathyroidism should be averted by early prevention of hyperphosphatemia through diet and phosphate ligants, and by normalization of the calcium balance through calcium supplements and vitamin D or its analogues. This treatment requires close clinical and laboratory control in order to avoid several hazards (hypercalcemia, hypophosphatemia, and refractory constipation). In cases with severe secondary hyperparathyroidism, subtotal parathyroidectomy is sometimes required. Nevertheless, in one such case this operation resulted in sudden hypoparathyroidism two years postoperatively.
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PMID:[Treatment of renal osteodystrophy: physiopathology and secondary effects]. 33 72

Previous nuclear disease was found twice: Mc Ardle disease, dermatomyositis. Causative factors were: strenous exercise, hyperthermia, intoxication, influenza. Myalgias and/or myoedema was recorded in ten cases, associated with an hypovolemia of variable severity in eight. Oligo-anuria was observed in eight cases. The acute renal failure (ARF) was characterized by an increase in the serum creatinin more important than the rise in the blood urea and, in some cases, severe metabolic disturbances: hyperkaliema (6 cases), hypocalcemia (5 cases), hyperphosphatemia (5 cases) and hyperuricemia (5 cases). Diagnosis was made by the increase in sera of the muscles enzymes, specially the CPK and the search for myoglobinuria, positive during the first seven days. A complete recovery of renal function was observed in the nine survivors with a transient and moderate hypercalcemia in three. Three patients had persistant neuro-muscular deficiencies. Non traumatic rhabdomyolysis is not a rare cause of ARF and should be considered when the etiology of ARF is uncertain.
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PMID:[Acute renal failure due to non traumatic rhabdomyolysis. 11 cases (author's transl)]. 53 Sep 46

White Leghorn chick embryos were injected on the 15th day of incubation with 70 to 300 pmoles 1,25-(OH)2D3. All doses produced hypercalcemia; with the highest dose, the concentration of calcium in serum started to rise 4 h after the injection, reached a peak 20 h after, and was still high 48 h after. Twenty hours after the injection of the same dose, the concentration of inorganic phosphorus in the serum was significantly lower than in the corresponding controls. The tibias from 17-day-old chick embryos injected with 300 pmoles on day 15 were shorter, lighter, and had a lower ash content than those from controls. Histological signs of resorption appeared to be reduced with respect to controls, but no precise quantitation was conducted. The fact that hypercalcemia was not accompanied by hyperphosphatemia may suggest that the vitamin stimulates resorption of calcium from the shell, which is mainly formed by calcium carbonate rather than from the bone from which calcium and phosphate are usually resorbed together.
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PMID:Effects produced by the administration of high doses of 1,25-dihydroxycholecalciferol to the chick embryo. 57 6

The present study is an investigation of the mechanism of hypercalcemia and hyperphosphatemia induced by the intravenous injection of lead acetate (Pb-Ac). A total of 118 male rats were injected with 30 mg/kg of Pb-Ac, or with 16.5 mg/kg of sodium acetate as the control. The levels of serum calcium, phosphorus and lead were then determined at various time periods after the injections. Serum calcium and phosphorus levels increased with time after Pb-Ac injection and the maximum values of calcium (17 mg%) were found after 1 h and of phosphorus (13.5 mg%) after 30 min. Both calcium and phosphorus levels reverted to the normal range after 12 h. The maximum net rates of increase of calcium and phosphorus were found immediately after Pb-Ac injection. At that time, deposition of lead at the calcifying sites of bone and incisor dentin was demonstrated by a histochemical examination. In other experiments the changes in the calcium and phosphorus contents in the medium after shaking bone powder in serum with Pb-Ac in an in vitro system were studied. It was confirmed that the calcium and phosphorus were displaced from the bone mineral, the extent of the displacement being correlated with the concentration of the Pb-Ac added to the medium, and that these displacements were very rapid reactions. These results suggest that hypercalcemia and hyperphosphatemia following Pb-Ac injection results from a direct action of lead on the bone mineral.
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PMID:Mechanism of induction of hypercalcemia and hyperphosphatemia by lead acetate in the rat. 59 44

The results of morphologic studies performed in 18 patients who had total parathyroidectomy and autotransplantation of parathyroid tissue into the forearm muscle are presented. All patients had long-standing renal disease with azotemia, hyperphosphatemia and high levels of parathyroid hormone. The histologic findings after total parathyroidectomy, before gland transplantation, are important for selection of parathyroid tissue for surgery. Diffuse hyperplasia with the development of multiple nodules of the parathyroids can possibly be adverse for the transplant. In one case, nine month after autotransplantation we found a tumor in the forearm, measuring 2.0 X 3.0 X 2.2 cm in diameter. Morphologic findings in this case before implantation showed diffuse hyperplasia with adenomatous nodules but no signs of carcinoma. The grafted parathyroid tissue after excision was seen with blood vessel invasion in the normal skeletal muscle. In the case of primary renal disease with secondary parathyroid hyperplasia, the light microscopic examination revealed an autonomous tumorlike adenomatous formation in the autografted parathyroid tissue, with graft-dependent hypercalcemia. The invasive growth with some signs of neoplasia following autotransplantation raises the question of the development of certain neoplasia.
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PMID:[Morphological aspects of parathyroid gland transplantation. Contribution on the clinical relevance of induced, invasive tissue growth]. 72 Jan 63

A 33 year old man presented with symptoms of one week's duration; he had a serum calcium of 22.5 mg/dl and a markedly hypercellular bone marrow. Despite therapy with saline diuresis, furosemide mithramycin, total parathyroidectomy and corticosteroids, symptomatic hypercalcemia was poorly controlled. Inappropriate serum parathyroid hormone (PTH) levels were found before and after parathyroidectomy whereas assays of the peripheral blood for osteoclast-activating factor and prostaglandin E (PGE2) were negative. An elevated leukocyte alkaline phosphate level, the inability to aspirate marrow, the marked generalized hyperplasia of all hematopoietic marrow elements, the focal accumulations of blastic cells and increasing reticulin fiber formation led to the diagnosis of acute myelofibrosis. A single course of cytosine arabinoside and thioguanine therapy was followed by profound hyperphosphatemia, hypocalcemia and death. The rarity of hypercalcemia with myeloproliferative disorders is documented by a review of the world literature, and the possible mechanism for hypercalcemia in this patient is discussed.
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PMID:Acute myelofibrosis and malignant hypercalcemia. 84 61

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


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