Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.3.1 (alkaline phosphatase)
 47,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Parathyroidectomy was carried out in 26 patients over a 14-year period. Excellent results were obtained in patients with severe hyperparathyroidism. Vascular calcification, hypercalcaemia and pruritus did not justify surgery unless associated with unequivocal hyperparathyroidism. 13 patients required intravenous calcium infusion for up to 2 weeks to control post-operative hypocalcaemia. Calcium requirements could be predicted from the pre-operative plasma alkaline phosphatase level. Following operation continued treatment with vitamin D was necessary to prevent hypocalcaemia. Hyperparathyroidism recurred in 1 patient after 8 years and 4 patients developed osteomalacia. Since parathyroid hormone may have toxic effects other than those on bone, maintenance of normal levels should be a long-term objective in the treatment of patients with chronic renal failure. Where large parathyroid glands are present, surgical reduction in gland mass is a logical prelude to long-term suppression of parathyroid hormone with vitamin D and phosphate-binding agents.
Nephron 1983
PMID:Parathyroidectomy in chronic renal failure. 668 30

A 1-year controlled trial was performed to confirm the effects of 1 alpha-hydroxycholecalciferol (1 alpha-OH-D3) in chronic hemodialysis patients. Initially, a daily dose of 2 micrograms of 1 alpha-OH-D3 was given orally to 24 patients and its placebo to another 24 patients during the first 3 months. For the following 9 months the dose of 1 alpha-OH-D3 or its placebo was reduced to 1 microgram per day in the individual groups. Serum calcium was significantly increased to the normal level after 1 month of treatment and sustained at this level for 1 year. Serum parathyroid hormone was significantly decreased at 3 months. Serum alkaline phosphatase was decreased to the normal level at the 5th month and thereafter. At 2 months serum phosphorus was significantly increased in the 1 alpha-OH-D3 group. None of the patients on 1 alpha-OH-D3 showed increased subperiosteal resorption on X-rays, whereas 8 out of 20 patients on placebo did (p less than 0.002). No adverse effects were seen apart from 3 patients with the 'red eye' of scleral calcification.
Nephron 1981
PMID:1-year controlled trial of 1 alpha-hydroxycholecalciferol in patients on maintenance hemodialysis. 702 62

In 27 patients with end-stage chronic renal failure an elevated calcitonin (CT) and parathyroid hormone was found. On stimulation with Ca i.v. there were 9 cases in whom delta CT proved to be higher than the maximal response of 50 pg ml-1 in controls. Supranormal CT responses were found predominantly in patients with normal alkaline phosphatase, who as a group increased their CT from 94.5 +/- 61 to 142.0 +/- 94 pg ml-1 (p less than 0.02). In contrast to this, patients with elevated alkaline phosphatase who also had a higher level of parathyroid hormone maintained unchanged CT on Ca stimulation. It is concluded that in chronic renal failure with severe secondary hyperparathyroidism, delta CT on stimulation is normal, while an enhanced delta CT often exists when hyperparathyroidism is of insufficient degree to cause a raised alkaline phosphatase.
Nephron 1982
PMID:Enhanced calcitonin release in chronic renal failure depending on the absence of severe secondary hyperparathyroidism. 712 54

Renal osteodystrophy in part due to secondary hyperparathyroidism, is one of the major unresolved problems affecting patients on chronic hemodialysis. In addition, evidence has shown that parathyroid hormone (PTH) is toxic to other organ systems besides bone. The results of a prospective study on the effect of propranolol in reducing PTH levels in chronic renal failure patients on hemodialysis are reported. Propranolol administration reduced PTH levels by over 50-75%. The levels of calcium, phosphorus, alkaline phosphatase and hematocrit were variable, but patients with severe derangements in these measurements also seemed to benefit from propranolol. It should now be determined by larger and longer studies whether these biochemical improvements can be translated into clinical benefits.
Nephron 1981
PMID:Suppression of secondary hyperparathyroidism by propranolol in renal failure patients. 721 43

Phosphorus (Pi) retention linked to chronic renal failure (CRF) favors secondary hyperparathyroidism (HPT). Reduction of Pi and protein intake has been shown to prevent the development of HPT in CRF. The aim of the present study was to assess in patients with advanced CRF the long-term effects on phosphate and calcium metabolism of a low-Pi (5-7 mg/kg/day), low-protein (0.4 g/kg/day) diet providing 300 mg/day calcium (Ca) and supplemented with amino acids and ketoacids, Ca carbonate (400-800 mg/day) and vitamin D2 (1,000 IU/day). Twenty-nine patients with advanced CRF (glomerular filtration rate (GFR) 13.7 +/- 4.5 ml/min) were selected for the study, on the basis of a follow-up of a least 2 years and a satisfactory compliance to the prescribed diet. At the start of the study, biological evidence of HPT was present with increased plasma PTH concentration (144 +/- 95 pg/ml), increased plasma Pi (1.57 +/- 0.33 mmol/l), an increase in alkaline phosphatase activity and plasma osteocalcin concentration. Plasma PTH concentration was positively correlated with plasma Pi and inversely with plasma Ca concentrations and GFR. Pi and protein restriction induced a significant correction of HPT within 3 months after starting the diet. After 2 years of diet, despite the diminution of GFR (11.1 +/- 3.7 ml/min, p < 0.0001), plasma PTH was still lower than at the start of the diet (88 +/- 57 pg/ml, p < 0.01), as was plasma Pi (1.32 +/- 0.24 mmol/l, p < 0.001), total plasma Ca being higher (p < 0.01). Plasma PTH levels were correlated only to plasma Ca concentrations.(ABSTRACT TRUNCATED AT 250 WORDS)
Nephron 1995
PMID:Long-term control of hyperparathyroidism in advanced renal failure by low-phosphorus low-protein diet supplemented with calcium (without changes in plasma calcitriol). 747 15

The effects of recombinant human erythropoietin (rHuEPO) treatment on parathyroid function in patients on maintenance hemodialysis (HD) with secondary hyperparathyroidism (HPT) is poorly understood. We compared the levels of serum intact parathyroid hormone (PTH) and the suppressibility of PTH by intravenous calcium infusion before and after 12 weeks of rHuEPO treatment in 8 HD patients with secondary HPT. The suppressibility of PTH by calcium infusion in HD patients was also compared with that of normal subjects. After rHuEPO treatment, in HD patients hematocrit and hemoglobin levels increased significantly from 20.1 +/- 1.3% and 6.65 +/- 0.46 g/dl to 28.7 +/- 1.0% and 9.68 +/- 0.39 g/dl, respectively. The serum intact PTH levels did not change significantly (541.9 +/- 65.3 pg/ml before versus 572.9 +/- 75.3 pg/ml after rHuEPO treatment), nor did serum ionized calcium, phosphate, magnesium, aluminum, alkaline phosphatase, and 1.25(OH)2D levels. Calcium infusion significantly increased serum ionized calcium and suppressed serum PTH levels. However, the increment in serum calcium levels and the percent decrement of serum PTH showed no significant differences before and after rHuEPO treatment in HD patients. Elevations in serum calcium levels during calcium infusions were not significantly different between normal subjects and HD patients. However, the percent maximal decrement in serum PTH level was less in HD patients both before and after rHuEPO treatment than in normal subjects (-75.4 +/- 3.9 and -76.4 +/- 4.1% versus -91.4 +/- 1.4%). We conclude that rHuEPO treatment has no influence on parathyroid function in maintenance HD patients with secondary HPT. In addition, PTH secretion is less suppressed by calcium infusion in the same group of patients.
Nephron 1995
PMID:Lack of influence of recombinant human erythropoietin on parathyroid function in hemodialysis patients with secondary hyperparathyroidism. 756 8

Male albino mice had one daily intraperitoneal injection of 4.25 g/100 ml glucose concentration fluid for peritoneal dialysis at pH 5.0-5.2, for a period of 30 days. At the end of the experimental periods, mesothelial cell imprints were taken from the peritoneal layer of the anterior liver surface. Histochemical staining of imprints obtained from mice exposed to the peritoneal dialysis fluid showed a consistently increased activity of: (a) enzymes associated with the cell membrane: Na-K-ATP-ase, alkaline phosphatase and 5-nucleotidase; (b) cytoplasmic enzymes: acid phosphatase and cytochrome oxidase, and (c) a modestly increased activity of glucose-6-phosphatase. These changes, which are not far from those observed in activated mesothelial cells, suggest that exposure of mesothelial cells to high glucose concentrations of PD fluid is associated with increased production and disposal of energy to be used for maintaining the constancy of the cellular environment and, probably, for fuelling the transcellular transport of solutes of large molecular size.
Nephron 1995
PMID:The cytochemical profile of visceral mesothelium under the influence of lactated-hyperosmolar peritoneal dialysis solutions. 777 14

To investigate the effect of rapid correction of chronic metabolic acidosis on circulating intact parathyroid hormone (I-PTH) activity by free calcium clamp in chronic renal failure, 18 patients were enrolled in this study. Metabolic acidosis was corrected by continuous bicarbonate infusion while plasma ionized calcium was clamped at the preinfusion level throughout the entire procedure. The plasma pH, bicarbonate, total CO2, sodium, serum total calcium and 1,25(OH)2 vitamin D3 levels increased significantly while serum concentrations of I-PTH, alkaline phosphatase and albumin showed significant decreases after bicarbonate infusion. The plasma ionized calcium, potassium, serum magnesium and inorganic phosphorus levels showed no significant difference before and after bicarbonate infusion. These results demonstrate that rapid correction of metabolic acidosis attenuates circulating PTH activity in chronic renal failure and may underline the importance of maintaining normal acid-base homeostasis particularly in the presence of secondary hyperparathyroidism.
Nephron 1994
PMID:Rapid correction of metabolic acidosis in chronic renal failure: effect on parathyroid hormone activity. 796 74

To determine the diagnostic role of urinary trehalase in chronic glomerular disease, urinary trehalase activity and other urinary markers such as N-acetyl-beta-D-glucosaminidase (NAG), alanine aminopeptidase (AAP), alkaline phosphatase (ALP), gamma-glutamyltranspeptidase (gamma-GTP), lactate dehydrogenase (LDH), lysozyme and beta 2-microglobulin (BMG) were measured in patients with chronic glomerulonephritis, nephrotic syndrome and chronic renal failure. Urinary trehalase activity was significantly increased in chronic glomerular disease, especially nephrotic syndrome, as compared with that in the healthy subjects. The highest incidence of elevated excretion was observed for trehalase with 52% in chronic glomerular disease, followed by NAG. Urinary trehalase activities in the patients were significantly correlated with the urinary levels of protein, NAG and AAP and total score of tubular damage, but not correlated with urinary levels of BMG or lysozyme. In patients with chronic glomerulonephritis and nephrotic syndrome, there was no significant difference in urinary trehalase activities between with and without hematuria. These results indicate that in some patients with chronic glomerular disease, there is tubular involvement as substantiated by elevation of the other urinary enzymes and BMG. Urinary trehalase is elevated more often in these types of disease than other markers of tubular damage.
Nephron 1993
PMID:Urinary trehalase activity in chronic glomerulonephritis. 809 31

A patient with impaired renal function, severe osteomalacia and aluminium intoxication is described. In response to Desferal (desferrioxamine) treatment, serum osteocalcin rose 8-fold whereas serum alkaline phosphatase and procollagen I peptide levels changed little. Chromatographic separation showed that the measured osteocalcin coeluted with intact osteocalcin. The osteocalcin in the serum probably comes from the liberation of pre-existing osteocalcin from the bone, concomitant with aluminium mobilisation, rather than by stimulation of de novo synthesis.
Nephron 1993
PMID:Anomalous rise of serum osteocalcin following desferrioxamine treatment in aluminium intoxication. 824 87


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