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)

Twenty-one patients with chronic renal failure and bone disease or hypercalcaemia were studied before and following single (twenty patients) or repeated (fourteen patients) intravenous injection of synthetic salmon calcitonin. Significant correlations were noted before treatment between bone surfaces occupied by osteoblasts or osteoclasts and plasma levels of immunoreactive parathyroid hormone, alkaline phosphatase and hydroxyproline. Following a single injection of 2--200 i.u. salmon calcitonin, plasma levels of calcium and phosphate fell for 6--8 h, but rose subsequently to pre-injection levels at 24 h. The magnitude and duration of the hypocalcaemic response was not clearly dose-dependent, but correlated with measured indices of bone cell activity. Repeated administration of calcitonin (10--200 i.u. thrice weekly for up to 2 months) lowered plasma calcium in the majority of patients and restored plasma calcium to normal in four previously hypercalcaemic patients. Mean levels of alkaline phosphatase increased but no significant changes in plasma phosphate, immunoreactive parathyroid hormone and calcitonin, or hydroxyproline occurred. Calcium absorption (six studies) did not change during treatment. We conclude that synthetic salmon calcitonin is an effective short-term inhibitor of bone resorption in patients with chronic renal failure. Its use as a possible treatment for hypercalcaemia and hyperparathyroid bone disease in chronic renal failure is discussed.
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PMID:Responses to salmon calcitonin in chronic renal failure: relation to histological and biochemical indices of bone turnover. 679 36

Bone Gla protein (BGP) was measured in the plasma by radioimmunoassay (RIA) during treatment of 59 patients with bone diseases including Paget's disease (N = 9), primary hyperparathyroidism (N = 25), chronic renal failure (N = 20), and cancer involving bone (N = 5). Plasma BGP was increased above normal in all patients. BGP decreased in the patients with Paget's disease following the acute and chronic administration of salmon calcitonin. Plasma BGP was higher in women then in men with primary hyperparathyroidism. Following parathyroidectomy, BGP decreased in both sexes but the decrease was significant in women only. Plasma BGP was increased in patients with renal osteodystrophy and did not change after hemodialysis. In the patients with bone cancer, plasma BGP decreased during treatment of the attendant hypercalcemia with salmon calcitonin. Although plasma BGP and serum alkaline phosphatase (AP) levels were generally correlated in these studies, there were examples of dissociation between the two. The measurement of plasma BGP appears to provide a specific index of bone metabolism that may in some circumstances be more sensitive than serum alkaline phosphatase measurement. However, further studies are necessary to establish the clinical value of plasma BGP measurement by RIA in the management of patients with bone diseases.
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PMID:Changes in plasma bone GLA protein during treatment of bone disease. 680 17

A patient with sarcoidosis and chronic renal failure was treated for hyperphosphatemia with aluminum hydroxide. The subsequent fall in serum phosphorus was followed by the development of hypercalcemia and nephrolithiasis. Corticosteroid therapy normalized the serum calcium and halted the progression of the nephrolithiasis, but did not improve renal function. Hyperphosphatemia may have blocked the expression of sarcoid hypercalcemia in the patient. The mechanism is unclear but inhibition of the synthesis or action of 1,25-dihydroxyvitamin D may have been involved. Reduction of serum phosphorus may lead to severe hypercalcemia in some patients with sarcoidosis.
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PMID:Hypercalcemia and nephrolithiasis provoked by serum phosphorus reduction in a patient with chronic renal failure and sarcoidosis. 684 58

Patients with end-stage renal failure develop osteodystrophy in part due to defective production of 1,25-dihydroxycholecalciferol by the kidney. We treated eight adults with chronic renal failure and osteodystrophy with 1,25-dihydroxycholecalciferol (calcitriol) for 30-44 months. Seven of these patients were also symptomatic with bone pain and/or muscle weakness. Striking amelioration of muscle weakness occurred, and bone pain was considered to be significantly improved in four of seven patients. Hypercalcemia was noted in all the patients, necessitating a reduction in the daily dose of calcitriol to a range of 0.125 to 0.5 microgram/day. While serum alkaline phosphatase fell during therapy, serum iPTH did not show any significant change. Bone mineral content improved in four patients, though it still remained below normal. Radiographic changes of osteodystrophy showed definite improvement in only three.
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PMID:Long-term therapy of uremic osteodystrophy in adults with calcitriol. 689 93

The long-term effects of vitamin D analogues and metabolites on renal function were assessed in 24 patients with and without chronic renal failure. Treatment for periods of 5-45 months did not adversely affect renal function in 10 of 11 patients with stable renal function, although transient hypercalcaemia did cause transient rises in plasma creatinine. Of 13 patients with progressive renal failure before treatment, vitamin D-like compounds or the vehicle used for their administration may have accelerated renal failure in 3 patients independently of changes in plasma calcium or phosphate. Particular difficulties in assessing the effects of vitamin D-like compounds in progressive renal disease are discussed.
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PMID:Effects of vitamin D metabolites and analogues on renal function. 689 66

The present study was aimed at answering the following two questions: (1) What is the effect of high dose vitamin D treatment on the serum level of 25-hydroxyvitamin D (25-OH-D) in patients with chronic renal failure (CRF)? (2) Is there any effect of urinary protein loss on the serum 25-OH-D levels during treatment with pharmacological doses of vitamin D? 42 patients with CRF were studied. They were treated conservatively by a low protein diet and received 15 mg of vitamin D2 once a week. Long-term administration of vitamin D caused a significant (5- to 7-fold) increase of plasma 25-OH-D level irrespective of the degree of proteinuria. This increase was noted only during the first 5 months of vitamin D2 treatment. Surprisingly only in some patients moderate hypercalcemia (> 2.75 mmol/l) was found. From the results obtained it is concluded that (1) patients with CRF differ from normal subjects in handling of high doses of vitamin D and (2) high dosage treatment with vitamin D may prevent hypocalcemia in patients with CRF in spite of high proteinuria.
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PMID:Serum 25-hydroxyvitamin D in patients with chronic renal failure on long-term treatment with high doses of vitamin D2. 696 39

Secondary hyperparathyroidism is a universal complication of chronic renal failure. It has been proposed that the markedly elevated levels of immunoreactive parathyroid hormone (i-PTH) in uremia may represent a "uremic toxin" responsible for many of the abnormalities of the uremic state. Plasma i-PTH consists of a mixture of intact hormone, a single-chain polypeptide of 84 amino acids, and smaller molecular weight hormonal fragments from both the carboxy- and amino-terminal portion of the PTH molecule. The hormonal fragments arise from metabolism of intact PTH by peripheral organs as well as from secretion of fragments from the parathyroid glands. The structural requirements for the known biological actions of PTH reside in the amino-terminal portion of the PTH molecule. Carboxy-terminal fragments, biologically inactive at least in terms of adenylate cyclase activation, hypercalcemia, or phosphaturia, depend on the kidney for their removal from plasma, and thus accumulate in the circulation in chronic renal failure. It is unknown at the present time if other biological effects of these carboxy-terminal fragments may contribute to some of the biochemical alterations observed in uremia. The most significant consequence of increased PTH levels in uremia is the development of bone disease characterized by osteitis fibrosa. In addition, it would appear that PTH plays an important role in some of the abnormal electroencephalographic patterns observed in uremia. This may be due to a potential role of PTH in increasing calcium content of brain. Parathyroid hormone also has been implicated as a pathogenetic factor in many other alterations present in uremia, i.e., peripheral neuropathy, carbohydrate intolerance, hyperlipidemia, and other alterations. Unfortunately, outstanding clinical research is lacking in this field and conclusive experimental data are practically nonexistent. Further studies are necessary if one is to accept the concept of PTH being a significant "uremic toxin."
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PMID:Parathyroid hormone metabolism and its potential as a uremic toxin. 699 9

In order to provide information about the prevalence of hypercalcaemia and its different causes, a retrospective survey was carried out in all hospital in-patients in whom serum calcium was elevated. Six hundred and forty-four cases were seen in two years and eight months, but a number of these were excluded as being spurious measurements leaving 496 cases of genuine hypercalcaemia. Four hundred and sixty-nine records (95 per cent) were successfully traced and analysed. Two hundred and nineteen cases of hypercalcaemia with malignancy were found together with 68 cases with chronic renal failure and 59 cases of primary hyperparathyroidism. In 102 cases no cause was identified.
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PMID:Hypercalcaemia--a hospital survey. 702 40

Six patients with stable end stage chronic renal failure have been studied while receiving keto-acid supplements that provided a daily calcium load of 42 +/- 2 mM. None of the patients had intercurrent illness. All patients showed elevated serum calcium concentration levels while on keto-acid supplements, reaching significance on 5 occasions. Reciprocal falls in serum phosphate concentrations were noted in all patients, and this observation was not due to an anabolic effect of the keto-acids. In 3 patients, the rise in serum calcium concentration was associated with marked clinical manifestations that required curtailment of treatment. The risk of hypercalcemia occurs early and certain high risk categories can be identified. Recommendations about the use of calcium salts of alpha-keto-acid analogues are given and it is suggested that a choice should be made available between calcium and sodium salt analogues.
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PMID:Changes in serum calcium caused by supplementation of low protein diets with keto-acid analogues in patients with chronic renal failure. 719 26

A model of chronic renal failure was created in nine adult sheep by two-stage, subtotal nephrectomy. Carotid-jugular cannulas provided clot-free access for 72 to 274 days without exit-site infections. All sheep became uremic and anemic. Median survival, while uremic, was 145 days (72 to 327 days), although three were sacrificed. Five required dialysis within the first week of uremia, and median survival on dialysis was 70 days (41 to 177 days). Sheep that maintained adequate nutrition survived the longest on dialysis. Mean creatinine and BUN levels in the stable uremic and dialyzed sheep were 4.8/95 and 7.8/59 mg/dl, respectively. The other serum chemistries remained unchanged (mean values) from normal, although one sheep died of hypercalcemia (17.8 mg/dl). Renal blood flow correlated to GFR in both normal and uremic states. GFR fell more than serum creatinine rose, suggesting extrarenal excretion of creatinine.
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PMID:Physiologic studies in normal and uremic sheep: I. The experimental model. 720 57


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