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

The relationship of sarcoidosis to renal insufficiency is not widely known by pathologists or clinicians. During an 8-year period beginning in 1980, we observed six patients with sarcoidosis and clinically significant renal insufficiency (serum creatinine, greater than 260 mumol/L). In one of these patients with long-standing sarcoidosis, renal insufficiency was attributed to unrelated primary renal disease until renal biopsy specimen showed interstitial noncaseating granulomas. The four patients with renal insufficiency at presentation differed from the typical patient with sarcoidosis because they were white men who lacked the usual clinical constellation of skin, eye, and pulmonary involvement. All four had noncaseating granulomas on their initial biopsy (bone marrow [3 patients], and lymph node [1 patient]), suggesting each had sarcoidosis, yet each had two or more follow-up biopsies before the diagnosis of sarcoidosis was accepted and appropriate therapy initiated. One of these four patients underwent long-term antifungal and antituberculous therapy. The major causes of renal insufficiency in these six patients were complications of hypercalcemia and interstitial granulomatous nephritis. Except in one patient with nephrocalcinosis, prednisone therapy resulted in a dramatic fall in serum creatinine level with resolution of hypercalcemia. Sarcoidosis is a rare, but treatable, cause of renal insufficiency. Early recognition by clinicians and pathologists may spare patients from undergoing unnecessary biopsies and result in more timely initiation of therapy.
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PMID:Renal insufficiency in sarcoidosis. A clinical and pathologic study. 233 57

We have studied the control of amino-terminal parathyroid hormone (PTH) secretion in haemodialysis patients in response to slow or fast calcium infusion and during acute hypocalcaemia. In nine patients, fast calcium infusion (0.4 mmol/kg bodyweight per hour) for 15 min increased ionised calcium and reduced PTH, with an initial t 1/2 of 12.8 min. After the infusion had ceased, calcium decreased steadily, and PTH increased, mean PTH reaching baseline values when calcium was still significantly greater than pre-infusion values. During slow calcium infusion for 2.5 h (0.1 mmol/kg bodyweight per hour), parathyroid suppression was evident at 15 min, when the calcium increment was only 0.03 mM. After 60 min, PTH did not decrease further despite progressive hypercalcaemia. Hypocalcaemic haemodialysis led to rapid increases in PTH. After 15 min, the mean calcium decrement was 0.09 mM (P less than 0.01) and the mean PTH increment was 283 pg/ml (P less than 0.01). The parathyroid response was maximal at 30 min, and did not increase subsequently, despite progressive hypocalcaemia for a further 90 min. During recovery from hypocalcaemia, PTH reduced and, despite comparable hypocalcaemia, PTH during periods of increasing calcium was always lower at a given calcium concentration than while calcium was decreasing. This influence of the direction of change of calcium was not seen during hypocalcaemia. The results showed that even in-advanced renal disease, the parathyroid glands are highly responsive to small initial increments (0.03 mM) and decrements (0.09 mM) in blood calcium, though less so to further perturbation of blood calcium.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of direction and rate of change of calcium on parathyroid hormone secretion in uraemia. 250 83

With increasing recognition of problems regarding the use of aluminum hydroxide as a phosphate binder, calcium carbonate has become the medication of choice. Use of calcium has, however, frequently been associated with development of hypercalcemia. At this institution, calcium carbonate powder as a phosphate binder, examination of its efficacy, and the frequency of hypercalcemia with its use were of great interest. Calcium carbonate powder (CalCarb-HD, 2.4 gms elemental calcium/packet) (CalCarb-HD, Lafayette Pharmacal Inc., Fort Worth, TX) was used in the study. Twenty-one end-stage renal disease (ESRD) patients (17 hemodialysis and 4 chronic ambulatory peritoneal dialysis) were chosen and converted from their previous binder (primarily, calcium carbonate tablets) to calcium powder. The dosage was adjusted to keep phosphorus levels at 3.5 to 5.5 mg/dl and calcium less than 11.5 mg/dl. At 2 months, the average calcium level in the 16 patients remaining in the study was 9.2 mg/dl, and the average phosphorus level was 5.2 mg/dl with an average calcium dose of 1.4 packets/day. By 7 months, the 8 patients remaining in the study had an average calcium level of 9.9 mg/dl with an average phosphorus level of 5.5 mg/dl; average calcium dose was 1.8 packets/day. Total episodes of hypercalcemia (calcium greater than 11.5 mg/dl) were two. Calcium carbonate powder appears to be an effective phosphate binder in the ESRD population. The relatively few episodes of hypercalcemia may be related to possible enhanced bioavailability of the compound secondary to its powdered form.
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PMID:Calcium carbonate powder as a phosphate binder. 259 73

We report two cases of patients with analgesic nephropathy presenting with the symptoms of hypercalcaemia, and who were found to have transitional cell carcinomas of the renal pelvis. On removal of the tumours, calcium levels fell to normal, indicating that a humoral factor produced by the tumour caused the hypercalcaemia. We suggest that hypercalcaemia in a patient with analgesic nephropathy may indicate a malignant change, and that serum calcium should be assessed when such patients are reviewed.
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PMID:Hypercalcaemia as a manifestation of malignant urothelial change in analgesic nephropathy. 271 Feb 70

Renal failure in patients with lymphoma or leukemia may be brought about by different causes, including ureteral obstruction, hypercalcemia, hyperuricemia, amyloidosis, immunologically mediated nephrosis and paraproteinemic nephropathy. Lymphomatous or leukemic infiltration of the kidneys is a frequent finding at autopsy but is rarely seen as a cause of renal failure. In this report three patients with lymphomatous infiltration of the kidneys causing renal failure are described. Clinical and laboratory criteria for establishment of diagnosis in such cases are suggested. Using these diagnostic criteria, a renal biopsy may not be necessary.
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PMID:[Renal insufficiency due to lymphomatous infiltration of the kidney: report of 3 cases and review of the literature]. 281 88

Calcium citrate was evaluated as a dietary phosphate binder in 81 patients with end-stage renal disease. These patients were grouped as follows: Group 1, 43 patients who were treated with calcium citrate; and Group 2 (the control group), 38 patients who were treated with aluminum-containing compounds. Blood chemistries were measured monthly and medications adjusted to maintain the following levels: serum calcium, greater than 9 mg/dl; serum phosphorus, less than 5.5 mg/dl; and total CO2 content, greater than 22 mmol/liter. At the end of the treatment period, the following serum values were obtained in Groups 1 and 2, respectively: calcium, 9.6 +/- 1.2 mg/dl (mean +/- SD) versus 8.9 +/- 0.8 mg/dl (P less than 0.001); phosphorus 5.5 +/- 1.9 mg/dl versus 7.0 +/- 2.3 mg/dl (P less than 0.005); and calcium-phosphate product, 52 +/- 18 versus 61 +/- 21 (P less than 0.05). Differences in alkaline phosphatase, total CO2 content, and C-terminal parathyroid hormone (C-PTH) values were not statistically significant between the two groups. Fifteen patients in Group 1 were then switched to aluminum-containing compounds and chemistries were compared one month later. During calcium citrate therapy, serum calcium was significantly higher, while C-PTH and serum alkaline phosphatase were significantly reduced. No difference was noted in serum phosphorous and total CO2 content. A questionnaire completed by 17 patients in Group 1 documented excellent patient tolerance to calcium citrate. Hypercalcemia (greater than 10.5 mg/dl) was the only significant complication, but only one patient became symptomatic. We conclude that, as a phosphate binder, calcium citrate is at least as effective as aluminum-containing compounds.
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PMID:Calcium citrate, a nonaluminum-containing phosphate-binding agent for treatment of CRF. 328 Aug 55

Endocrine disorders affecting the elderly present a continuing challenge to the clinician. Often confused with normal age-related changes or age-prevalent disease, disorders such as thyrotoxicosis, hyperglycemia, and hypercalcemia often go undetected until late in their course, if at all. Non-specific and atypical presentations make the diagnosis even more difficult and a low threshold for obtaining laboratory testing is advised. Thyrotoxicosis may present with only anorexia, weight loss, and cardiac dysfunction. Hyperglycemia often remains undetected; long-term sequelae, however, may impair function and result in problems such as neuropathy, postural instability, and nephropathy--conditions often dismissed as consequences of old age. Hypercalcemia may not present with the classic findings of renal colic, GI pathology, and skeletal disease. An acute confusional state with or without volume depletion appears to be a more frequent presentation during later life.
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PMID:Atypical presentation of endocrine disorders in the elderly. 338 39

Primary hyperparathyroidism results from autonomous secretion of parathyroid hormone by a single or multiple parathyroid glands. Clinical signs result from various combinations of hypercalcemia, hypercalcemic nephropathy, urolithiasis, or mobilization of calcium and phosphorus from bone. Following parathyroidectomy, the prognosis for dogs with primary hyperparathyroidism is good if the disorder is diagnosed before renal disease is advanced.
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PMID:Canine primary hyperparathyroidism and its association with urolithiasis. 351 5

Hyperparathyroid crisis secondary to primary hyperparathyroidism has variously been described as hypercalcemic crisis, parathyroid storm, and parathyroid intoxication as well as other equally descriptive terms. Whatever the nomenclature, all emphasize the seriousness and urgency of the condition. Although fewer than 200 cases have been described since the first report by Hanes in 1939, it is generally agreed that hyperparathyroid crisis is more prevalent than commonly appreciated. The signs and symptoms of the syndrome are believed due not only to the presence of hypercalcemia, but to the toxic effects of parathormone as well. Its wide, but nonspecific clinical spectrum makes it easily confused with other causes of rapidly fatal cardiovascular or renal disease. The mortality in untreated cases is essentially 100 per cent. With combined medical-surgical treatment, it is still reported as high as 60 per cent. Three patients with severe hyperparathyroid syndrome are reported. Effective control of both hypercalcemia and the toxic effects of acute hyperparathyroid crisis was achieved with the use of parenteral cimetidine. Definitive surgical removal of a solitary parathyroid adenoma was performed in all three patients. The intimate relationship of the bioavailability of cimetidine and its effect in primary hyperparathyroidism is clearly demonstrated. An analogy to the use of cimetidine in Zollinger-Ellison syndrome is made. Both are endocrinopathies that require doses of cimetidine in excess of that normally considered therapeutic for peptic ulcer disease. The signs and symptoms of hyperparathyroid crisis as well as current modalities of treatment are reviewed. It is concluded that parenteral cimetidine is an important aid in the management of acute hyperparathyroid syndromes secondary to primary hyperparathyroidism.
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PMID:Hyperparathyroid crisis reviewed: a role for parenteral cimetidine? 352 23

The metabolic manifestations and operative findings in 10 patients with a diagnosis of parathyroid carcinoma were analyzed to determine whether they differ from those in patients with parathyroid adenomas and similar degrees of hypercalcemia. Two groups of patients with parathyroid adenomas were used for comparison. Group A consisted of eight patients with "atypical" benign adenomas (mean preoperative level of serum calcium: 13.4 mg/dl); group B consisted of 13 patients with benign typical adenomas--all with preoperative serum calcium levels greater than or equal to 13.0 mg/dl (mean: 14.2 mg/dl). The patients with carcinoma (mean preoperative level of serum calcium: 15.3 mg/dl) had a frequency of osteoporosis and osteitis fibrosa cystica (50%) comparable with that of group A (33%) and group B (62%). Seventy percent of the patients with carcinoma had renal disease (nephrolithiasis, nephrocalcinosis, or impaired renal function), whereas only 38% of group A and 15% of group B had similar disorders. The patients with carcinomas had the highest frequency of combined bone and renal disease (50% versus 14% in group A and 15% in group B). Anemia, peptic ulcer disease, and hypertension occurred with similar frequencies in the three groups. Three patients with recurrent parathyroid carcinoma died of profound hypercalcemia, renal failure, or cardiac arrhythmia. In general, although patients with parathyroid carcinomas have more profound metabolic abnormalities than do patients with primary hyperparathyroidism, the metabolic manifestations in patients with parathyroid carcinoma are comparable with those in patients with parathyroid adenomas and profound hypercalcemia. Furthermore atypical adenomas share many anatomic and histopathologic features with parathyroid carcinomas, and distinguishing between the two is sometimes possible only in cases of tumor recurrence.
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PMID:Parathyroid carcinoma versus parathyroid adenoma in patients with profound hypercalcemia. 358 61


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