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 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

Six patients with biopsy-proven renal sarcoidosis presented with renal failure of unknown origin; in none was the diagnosis of sarcoidosis initially considered. The serum creatinine concentration at the time of presentation ranged from 265 to 1380 mumol/l (3.0 to 15.6 mg/dl), with a mean of 787 mumol/l (8.9 mg/dl). Although only two patients were hypercalcemic at the time of presentation, the 24-hour urinary excretion of calcium was increased in three of the four patients in whom it was measured, and renal calculi were present in one case. Renal biopsy revealed interstitial nephritis and tubular atrophy in all cases, as well as nephrocalcinosis in three cases and noncaseating granulomas negative for acid-fast bacilli in four cases. In each patient steroid therapy led to a rapid improvement in renal function (mean post-treatment serum creatinine level 274 mumol/l [3.1 mg/dl]). The follow-up period ranged from 8 months to 8 years (mean 3.0 years). In three patients renal function remained stable with low-dose steroid therapy. In two cases recurrent hypercalcemia and deteriorating renal function accompanied steroid withdrawal but resolved with its reinstitution. In one additional case reversible deterioration in renal function accompanied tapering of the steroid dose; however, there was no hypercalcemia.This report emphasizes the importance of considering sarcoidosis in the differential diagnosis of acute renal failure of unknown origin. Long-term follow-up of such patients is essential, as relapse is common.
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PMID:Clinical and pathological features of six cases of sarcoidosis presenting with renal failure. 51 62

Despite the high frequency of skeletal metastases from cancer of the prostate, hypercalcaemia is extremely uncommon in this condition. In two patients with advanced, poorly differentiated metastasizing cancer a fairly uniform clinical picture developed, with anaemia, leukocytosis, increased serum creatinine, thrombocytopenia, elevated alkaline and acid phosphatase levels and symptoms secondary to hypercalcaemia. The development of more effective agents against cancer of the prostate will probably afford longer palliation, but evidently at a risk of severe metabolic disturbances in the preterminal state.
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PMID:Advanced cancer of the prostate combined with hypercalcaemia. 59 76

Between 1972 and 1976 15 patients with chronic renal failure of different aetiology and varying severity were observed who developed 23 hypercalcaemic phases during treatment with calcium-containing drugs. 12 instances of hypercalcaemia occurred during conservative treated during conservative treatment (serum creatinine 177-1061 mumol/l, equivalent to 20-120 mg/l) and 11 during chronic haemodialysis (serum creatinine 707-1061 mumol/l, equivalent to 80-120 mg/l). In 15 cases hypercalcaemia was caused by a hexacalciumhexasodium-heptacitratehydrate complex (Acetolyt), in 6 cases by the combined use of this drug with calcium ion-exchange resins on a calciumpolystyrolsulfonate base, and in two cases by the use of calcium tablets and calciumpolystyrolsulfonate, respectively. The daily doses of these drugs were in the usual therapeutic range in most cases. Deterioration of renal function was observed in two cases and coma in a further two cases. In 5 cases gastric ulcers were demonstrated. Three patients died. In no patient was there evidence of florid hyperparathyroidism. Treatment with calcium-containing drugs in patients with renal failure should only be carried out under regular control of calcium concentrations.
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PMID:[Hypercalcaemic crises in patients with chronic renal failure caused by ion-exchange resins, antacidotics and other calcium-containing drugs (author's transl)]. 59 99

Chronic administration of lithium salts is associated with hypercalciuria in the rat. To study the renal and extrarenal mechanisms of this phenomenon, we utilized balance and clearance techniques in rats pair-fed diets with or without Li2CO3 (0.5 meq/day per rat). Lithium induced hypercalcemia (mean +/- SE: 5.40 +/- 0.09 VS. 5.06 +/- 0.05 meq/liter) and hypercalciuria (Ca/creatinine = 0.28 +/- 0.04 vs. 0.13 +/- 0.03) only during feeding. When CaCO2 supplement to a calcium-deficient diet was abruptly withdrawn, hypercalciuria was abolished. However, polyuria and polydipsia persisted. No significant changes in serum phosphate, urine phosphate, sodium, pH, or citrate were observed. Chronic parathyroidectomy (PTX) also abolished this effect. During clearance studies, fasting excretion of calcium was similar between treated and control animals. Superimposed acute PTX resulted in comparable changes, hence arguing against primary changes in renal calcium reabsorption or changes in parathyroid hormone effects on the renal tubule. Thus, lithium produces absorptive hypercalciuria by a mechanism dependent on intact parathyroid glands and adequate diet calcium, but independent of urine sodium, phosphate, or pH. The active component of gut calcium transport may be involved, possibly via alterations of vitamin D metabolism.
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PMID:Mechanism of lithium-induced hypercalciuria in rats. 62 44

Parathyroid hormone (PTH), creatinine, calcium and phosphate blood levels were repeatedly measured in 5 patients with acute renal failure. 1 patient developed hypercalcemia during the recovery phase of the illness. PTH was elevated in all cases before starting hemodialysis treatment and returned to normal when renal function recovered. Calcium and PTH were inversely correlated in 3 patients including the patient with transient hypercalcemia. These data show that parathyroid function in acute renal failure is closely related to changes in renal function and the hypercalcemia, when occurring, is not necessarily due to parathyroid hyperactivity.
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PMID:Parathyroid hormone and calcium blood levels in acute renal failure. With special reference to one patient developing transient hypercalcemia. 63 17

The influence of hypercalcemia on renal function was studied retrospectively in 13 patients suffering from primary hyperparathyroidism, sarcoidosis, vitamin D intoxication, malignant lymphoma or chronic lymphatic leucemia. Different kinds of treatment, depending upon the primary disease, often induced a rapid fall in the serum calcium concentration. The serum creatinine concentration always fell simultaneously. The serum phosphate concentration fell in all but two patients. Changes in serum calcium and serum creatinine correlated significantly (p less than 0.001), as did changes in serum calcium and serum phosphate concentrations (p less than 0.05). Serum calcium/serum creatinine and serum calcium/serum phosphate ratios were significantly higher in patients with primary hyperparathyroidism than in patients with hypercalcemia of non-hyperparathyroid origin (p less than 0.01, p less than 0.001). This suggests a different effect of calcium on the glomerular filtration rate in hyperparathyroid and non-hyperparathyroid patients, the latter group being more sensitive to the influence of hypercalcemia. Possible explanations for this difference, such as a protective effect of PTH on the glomerular filtration, are discussed.
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PMID:Reversible renal failure caused by hypercalcemia. A retrospective study. 64 44

Immobilization hypercalcemia following a single limb fracture of one weight bearing bone has been reported rarely in the pediatric age group. Nevertheless, in six of 12 patients immobilization hypercalcemia developed, associated with elevations in the urinary calcium/creatinine ratio and serum levels of ionized calcium after a single limb fracture of a weight-bearing bone during this two-year study period. We suggest that immobilization hypercalcemia occurs frequently in both children and adolescents after a single limb fracture of one weight-bearing bone, exercises in bed fail to prevent immobilization hypercalcemia, serial measurements of the serum ionized calcium and the urinary calcium/creatinine ratio are critical measures in treating such patients, and though complete mobilization is curative, transient calcitonin therapy is highly effective in reversing the disorders in calcium metabolism.
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PMID:Immobilization hypercalcemia after single limb fractures in children and adolescents. 65 37

Comparisons of isonitrogenous supplements (1.2 g N) of essential amino acids and five keto acid analogues with four essential amino acids were made in seven patients with stable chronic renal failure (creatinine clearance, 4.6 to 16 ml/min) on moderately protein-restricted diets (4.60 to 7.8 g N per day). Full nitrogen balance data on the four patients who have already completed studies lasting 24 weeks are presented. No benefits of keto acid over amino acid supplements were observed. Two transient episodes of hypercalcemia occurred during keto acid treatment. There was no improvement of renal function with keto acids. Also, no carry-over effects were seen after keto acid treatment. It is concluded that any beneficial effects of keto acids in patients with chronic renal failure are only likely to occur in those taking a diet of less than 30 g protein daily.
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PMID:Comparison of the effects of keto acid analogues and essential amino acids on nitrogen homeostasis in uremic patients on moderately protein-restricted diets. 70 31

Eighty-seven children less than 16 years of age with recent spinal cord injury were studied during a 7-year period (1970--1976). Serum calcium concentration was determined at least once in each of 76 of these patients, and in 18 (23.6%) it was above 11 mg%. Fifteen of the 18 patients had quadriplegia and 3 had paraplegia. In 5 patients, the first symptoms of acute hypercalcemia simulated those of an acute abdomen. Two of the 5 patients underwent exploratory laparotomy, with negative findings. The incidence of urinary stones was 55% (10 of the 18), a difference from the control population of only 18%. Hypercalcemia in the acute phase was almost always accompanied by decreased renal function characterized by inability to concentrate the urine and low corrected creatinine clearance. The treatment with saline infusions and furosemide was usually effective.
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PMID:Hypercalcemia in children with spinal cord injury. 71 6


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