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)

Delayed hypercalcemia developed in two patients with acute renal failure and rhabdomyolysis. In patient 1, the hypercalcemia appeared 14 days after the beginning of the diuretic phase of the illness and was associated with severe diastolic hypertension and soft-tissue calcification, including the lungs and skeletal muscles. The blood levels of 25-hydroxyvitamin D (25OHD3) were elevated during the hypercalcemia and decreased to normal when the patient became normocalcemic. In patient 2, the hypercalcemia occurred 55 days after the start of the diuretic phase and at a time when renal function was normal.
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PMID:Delayed hypercalcemia with acute renal failure associated with nontraumatic rhabdomyolysis. 697 99

Traumatic rhabdomyolysis with myoglobinuria and renal failure has been recognized for many years. In the past decade, rhabdomyolysis has been found to have various nontraumatic causes as well, including genetic conditions, metabolic disorders, exercise, toxins, infections, and drugs. Characteristic clinical and laboratory features include muscle tenderness, pigmenturia with urine that is orthotoluidine (Hematest) positive, greatly elevated creatine kinase levels, and often, renal failure. Treatment consists of fluid replacement and establishment of adequate urine flow early. If acute renal failure occurs, it should be treated appropriately. Particularly important are reversal of hyperkalemia and withholding of calcium during the hypocalcemic phase to prevent exacerbation of hypercalcemia later.
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PMID:Rhabdomyolysis as a cause of acute renal failure. 714 78

Rhabdomyolysis occurred in 25 of 1,000 patients (2.5%) with phencyclidine (PCP) intoxication. 10 of these 25 patients (40%) developed acute renal failure and another 7 had mild impairment in renal function. Marked hyperuricemia was present in all 17 patients, and marked hyperphosphatemia and hypocalcemia were noted in the 10 patients with acute renal failure; 3 of the latter developed hypercalcemia during the diuretic phase of the illness. Fever, tachycardia and hypertension were frequent findings among the 25 patients with rhabdomyolysis and all had leukocytosis. The data show that rhabdomyolysis with and without acute renal failure is not infrequent among abusers of PCP.
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PMID:Rhabdomyolysis with and without acute renal failure in patients with phencyclidine intoxication. 734 47

A 38-year-old man developed symptomatic hypercalcemia during the diuretic phase of acute renal failure secondary to rhabdomyolysis. Although early secondary hyperparathyroidism was documented, parathyroid hormone levels fell when hypercalcemia occurred. The 25-hydroxycholecalciferol level was normal on two separate occasions during the hypercalcemia. Remobilization of muscle calcium deposits during diuresis is proposed as the cause of the hypercalcemia in this syndrome.
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PMID:Parathyroid hormone and 25-hydroxycholecalciferol levels in hypercalcemia of acute renal failure. 736 60

Acute renal failure due to multiple myeloma is uncommon but may be the presenting feature of the disease. When it occurs, the underlying multiple myeloma is usually easily diagnosed by the presence of a serum M protein, hypercalcemia, skeletal pain, or typical bone lesions. We report here four cases of patients who, at the time they developed acute renal failure, had none of these findings nor any other historical or physical evidence of multiple myeloma. A renal biopsy in all four cases revealed the typical diagnostic features of "myeloma kidney" and led to confirmation of the diagnosis by bone marrow examination. Tamm-Horsfall protein was identified within myeloma casts and the glomerular urinary space, suggesting that tubular obstruction and retrograde urine flow precedes the development of "myeloma kidney" and acute renal failure.
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PMID:Renal biopsy diagnosis of clinically silent multiple myeloma. 739 12

Thirty patients with drug associated acute nontraumatic rhabdomyolysis were evaluated. Acute renal failure, oliguric (ORF) in ten and nonoliguric (NORF) in another ten patients, was observed. The remaining ten patients did not develop renal failure (NRF). To identify factors that may have contributed to this clinical diversity, these three groups were compared. Data from 51 patients reported in the literature were also included in the analysis. The patients with ORF were slightly younger than patients with NORF. They had higher incidence of muscle swelling and higher serum potassium. ORF was more severe, lasted longer, and required more dialysis than NORF. The group of patients with renal failure had higher incidence of coma and more patients with very high muscle enzyme elevation than NRF patients. Hypercalcemia, a unique complication of rhabdomyolysis, was reported in 22 patients. It was not seen in patients without renal failure. There were no differences in age, incidence of coma, muscle swelling, and muscle enzyme between those who did and those who did not develop hypercalcemia. Sixteen patients with nerve entrapment had higher incidence of coma and muscle swelling than the rest of the patients.
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PMID:Acute drug-associated rhabdomyolysis: an examination of its diverse renal manifestations and complications. 743 19

In a patient recovering from acute renal failure, hypercalcemia abruptly developed at a time when the serum creatinine level remained high (5 mg/dl) but well after the serum phosphate level had been restored to normal by oral aluminum hydroxide therapy. The renal damage had been severe, with oliguria lasting six weeks. Parathyroid hormone (PTH) immunoreactivity was measured with two different "carboxyterminal" PTH assays, giving high-normal or slightly mild renal failure could have accounted for the increased immunoreactivity. After five months of hypercalcemia, prednisone was administered and produced a prompt and sustained normalization of serum calcium. This prolonged variant of hypercalcemia after renal failure is not well recognized in the literature. The response to glucocorticoids suggests that abnormal metabolism of vitamin D or osteoclast activating factor might be involved in its genesis.
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PMID:Hypercalcemia after acute renal failure. 744 7

Cimadronate (YM175) is a novel bisphosphonate with potent inhibitory activity on bone resorption under development for the treatment of tumor-induced hypercalcemia, metastatic bone disease and osteoporosis. We conducted intravenous single and repeated dose toxicity studies of cimadronate in beagle dogs. In the single dose study, animals received a single dose of 0.3, 1, 3 or 10 mg/kg of cimadronate and the animals were observed for at least 14 days. At 10 mg/kg, both the male and female dog showed toxic signs such as vomiting, decreased locomotor activities and hypothermia and were killed in extremis within a week after dosing. In the 30-day study, animals received cimadronate at a dosage of 0 (vehicle), 0.03, 0.1, 0.3 or 1 mg/kg/day. At 0.03 mg/kg/day or more, histological findings indicated an increased amount of primary spongiosa in the rib and ilium. At 1 mg/kg/day, degenerative nephropathy, aggregation of spermatozoa and glandular hypoplasia of the prostate gland were observed. On day 16 of dosing one male animal died of acute renal failure. In the 26-week study, animals received cimadronate once weekly at a dosage of 0 (vehicle), 0.31, 0.62, or 1.25 mg/kg. Histopathological examination showed an increased amount of primary spongiosa in the rib at all dosage levels. In addition, similar findings were observed in the lumbar vertebrae at 1.25 mg/kg/week. Histopathological changes in the kidney and male reproductive organs were not observed.
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PMID:Intravenous single and repeated dose toxicity studies of cimadronate (YM175), a novel bisphosphonate, in beagle dogs. 749 Jul 87

7 acute renal failure (ARF) and experiments provided information on ARF induced by radio-opaque substances and indomethacin. The leading mechanism underlying renal failure is supposed to be the spasm of renal afferent arterioles secondary to hypercalcemia, prostaglandin synthesis blockade, activation of renin-angiotensin system and high activity of adenosine.
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PMID:[Acute kidney failure related to the use of x-ray contrast agents and indomethacin: the risk factors and mechanisms of its development]. 763 75

Disturbances in calcium metabolism in acute renal failure (ARF) remain incompletely understood. Most data are from patients with rhabdomyolysis. As renal impairment commonly accompanies severe malaria in the absence of rhabdomyolysis, falciparum malaria provides an alternative model of mineral homoeostasis in ARF. We studied 25 Vietnamese subjects, aged 18-63 yr, with severe malaria and 10 controls. Fourteen patients had a serum creatinine level of 250 mumol/L or less during treatment (group 1), five developed ARF but were not dialyzed (group 2a), and six required dialysis (group 2b). Group 1 patients presented with mild hypocalcemia (mean +/- SD serum ionized calcium, 1.18 +/- 0.05 vs. 1.23 +/- 0.02 mmol/L in controls; P = 0.01) that persisted until discharge in the presence of normal serum phosphate, PTH, and vitamin D metabolite levels. Group 2 patients were more hypocalcemic on admission (1.10 +/- 0.08 mmol/L; P < 0.0001 vs. controls), especially those in group 2b whose serum ionized calcium fell to 0.88 +/- 0.13 mmol/L when renal dysfunction was maximal. In group 2 patients, the admission serum PTH level was raised (5.4 +/- 3.8 vs. 2.7 +/- 0.9 pmol/L in controls; P < 0.02) and changed reciprocally with calcemia. Significant rises in serum phosphate occurred only in group 2b patients who had depressed serum free 1,25-dihydroxyvitamin D levels throughout. Hypercalcemia did not accompany the diuretic phase of ARF. These data suggest that parathyroid gland dysfunction is a cause of hypocalcemia in severe malaria without ARF, as seen in group 1 patients; in patients with ARF, the effect of the combination of phosphate retention and altered vitamin D metabolism on skeletal PTH sensitivity is of prime significance.
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PMID:Mineral homoeostasis in acute renal failure complicating severe falciparum malaria. 767 21


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