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

Electrolyte disturbances in leukemia can be the result of the disease process or drug therapy. One group of electrolyte abnormalities is related to the stage of the leukemic process. Included in this group are newly diagnosed patients who may show elevated serum potassium, phosphorus, and magnesium--a result of their release from malignant cells after cytotoxic therapy or their accumulation due to urate nephropathy. Patients in remission usually have normal serum electrolyte concentrations, but acute leukemia patients during relapse may have hypokalemia, hypophosphatemia, and hypomagnesemia. This imbalance may be related to cellular uptake of these electrolytes in the presence of inadequate dietary intake. Other factors contributing to electrolyte derangements, and related to the leukemic process, include hyponatremia and hypochloremia secondary to the SIADH, hypokalemia in acute monocytic or acute myelomonocytic leukemia due to lysozyme-induced tubular damage, hypercalcemia possibly secondary to leukemic infiltration of bone or parathyroid glands (with PTH release), or production of a PTH-like substance by leukemic cells. Nonspecific factors related to the disease process which may aggravate the electrolyte imbalance include gastrointestinal loss through nausea, vomiting, and malnutrition. The drug-related electrolyte abnormalities include cyclophosphamide- and vincristine-induced SIADH; decreased serum sodium, chloride, potassium, and calcium concentrations as a result of polymyxin B nephrotoxicity; hypokalemia and hypomagnesemia secondary to amphotericin B; hypocalcemia, hypophosphatemia, and hyperphosphaturia due to L-asparaginase-induced hypoparathyroidism; hypokalemia due to a nonreabsorbable anion effect of antibiotics in the distal tubule or changes in membrane ionic transport of all cells by large doses of antibiotics. Electrolyte disturbance in leukemia thus have a multifactorial pathogenesis which can best be delineated according to the stage of the leukemic process and the drugs being used. Recognition of the cause or causes in a particular patient is essential for an effective approach to management. This review emphasizes the need for routine measurement of serum electrolytes during all phases of the leukemic process.
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PMID:Electrolyte and acid-base disturbances in the management of leukemia. 26 90

Four cases of wide-spread arterial calcifications and peripheral necroses developing after successful renal transplantation are presented. In two cases parathyroidectomy was performed to prevent progress of the peripheral ischemic ulcers. In one of these cases, this was followed by healing of the necroses. In the two other cases parathyroidectomy had been performed because of hypercalcemia in the post-transplantation period. Ischemic ulcers appeared in these patients during treatment with vitamin D and healed after withdrawal of this therapy. Prevention of uremic arterial disease might be obtained by early control of serum phosphate levels and by renal transplantation at an early stage of renal disease. Parathyroidectomy should be considered in the treatment of developing peripheral gangrene in uremic patients and renal transplant recipients. Also, there are obvious hazards connected with vitamin D therapy in these patients.
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PMID:Arterial disease with ischemic ulcerations in renal transplanted recipients. 35 7

A 65-year-old woman with a history of a left heminephrectomy for renal carcinoma developed hypercalcaemia 11 years after the operation. The same kidney was found to contain a recurrent renal carcinoma. After the radical nephrectomy of the left kidney, hypercalcaemia remitted but reappeared 11 months later. The right kidney was small but functioned at a level of creatinine clearance of 10--15 ml/min. Metastatic work-up was negative, and secondary causes of hypercalcaemia were excluded. A neck exploration revealed a parathyroid adenoma. With parathyroid resection the serum calcium declined to normal, and the risk of hypercalcaemic nephropathy in the remaining kidney was precluded.
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PMID:Hypercalcaemia due to hyperparathyroidism in a patient with chronic renal failure and renal carcinoma. 42 90

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

Dogs given excess vitamin D (500 or 1,000 micrograms/kg of body weight each day for 1 to 3 weeks were observed for clinical and pathologic changes of increased blood pressure and of characteristic nephropathy associated with vitamin D toxicosis or hypercalcemia. Serum calcium and serum urea nitrogen (UN) increased throughout the treatment period, but serum phosphorus remained within the normal range. Plasma renin activity increased markedly. Blood pressure showed only insignificnat changes (P = greater than 0.05). Gross and microscopic examination of the kidneys suggested vascular-oriented changes with an ischemic basis. Glomerular vascular poles showed hypertrophy and hyperplasia of juxtaglomerular cells. Ultrastructually, an increase in the number of secretory granules was noticed in these cells. A hypothesis regarding the mechanism of renal injury during vitamin D toxicosis is presented.
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PMID:Vitamin D intoxication and the pathogenesis of vitamin D nephropathy in the dog. 45 87

A 4-year Basset bitch with a 9-week history of depression, lethargy, inappetence and weight loss was found to have azotaemia, hypercalcaemia and hyperphosphataemia. Laparotomy and kidney biopsy revealed end-stage renal disease and the dog was killed. Hyperplasia of all 4 parathyroid glands was found at autopsy. The presumptive diagnosis was idiopathic renal failure with resulting tertiary hyperparathyroidism.
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PMID:Renal failure, hyperparathyroidism and hypercalcaemia in a dog. 46 39

Acute renal failure may be a contributory cause of death in patients with acute leukemia. The purpose of this study was to define the causes and course of acute renal failure in group of patients with acute leukemia in order to identify preventive measures and reversible aspects of the renal insufficiency. Among 88 patients with acute leukemia whose courses were followed to the time of death, ten developed acute renal failure. Etiologic factors of the renal failure were uric acid nephropathy, sepsis with complicating hypotension and hypovolemia, and the administration of nephrotoxic antibiotics. In one patient ureteral obstruction from clots was responsible for renal failure, while in another patient disseminated aspergillosis led to renal failure. Other causes of acute renal failure in persons with acute leukemia, but not observed in this patient group, are hypercalcemia and leukemic infiltration of the kidneys.
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PMID:Acute renal failure in patients with acute leukemia. 63 12

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

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

A 25-year-old white woman with sporadic hypophosphatemic rickets presented with a 7 year history of chronic mild hypercalcemia, osteitis fibrosa cystic and hypercalcemic nephropathy. Serum immunoreactive parathyroid hormone was elevated by greater than 100-fold and a 3.5 g parathyroid tumor was found at operation. Survey of the literature reveals that of 9 previous cases in which hypercalcemic hyperparathyroidism occurred in association with hypophosphatemic rickets, only two had classical x-linked familial hypophosphatemic rickets. It appears more than likely that this unusual combination of skeletal diseases represents the chance occurrence of primary hyperparathyroidism in patients with underlying x-linked familial hypophosphatemic rickets rather than a complication of phosphate therapy.
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PMID:Hypercalcemic hyperparathyroidism in hypophosphatemic rickets. 87 68


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