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)

29 patients receiving haemodialysis treatment for chronic renal failure were divided into two groups on the basis of the presence or absence of bone disease as defined by radiology and bone alkaline phosphatase. The group of patient with bone disease showed a significantly greater increase in protein-bound calcium during dialysis compared with the control group. There were no significant differences in the changes in total calcium, albumin or hydrogen ion concentration during dialysis between each group. The data suggest that there is a relationship between the increase in protein-bound calcium during dialysis and the incidence of bone disease.
Nephron 1979
PMID:Changes in protein-bound calcium during haemodialysis in relation to bone disease. 3 10

The role of metabolic acidosis in the genesis of renal osteomalacia was investigated by studying bone mineralisation and resorption rates with a combined isotope and balance technique in six patients, before and after the administration of alkali. Correction of blood pH was achieved in five cases and was associated with a significant rise in the bone mineralisation rates and a significant positive trend in the calcium balances. It is suggested that acidosis contributes to the pathogenesis of osteomalacia in renal failure by slowing skeletal mineralisation, possibly by inhibiting bone alkaline phosphatase.
Nephron 1975
PMID:Effect of correction of metabolic acidosis on bone mineralisation rates in patients with renal osteomalacia. 23 58

The effects of synthetic salmon CT, administered subcutaneously and intermittently (1 MRC U/kg/day for 15 days/month over 6 months) were investigated in 15 uremic patients on regular dialysis treatment (RDT), all presenting various degrees of osteodystrophy. Clinically, osteoarticular pain disappeared in 8 out of 10 cases; 1 patient with rib fractures had a rapid calcification of the bone fracture repair tissue. No significant changes were found in serum calcium and PTH levels. Phosphotemia showed a significant decrease within the first 20 days. The varying individual hypophosphatemic response proved to be related to the initial level of phosphatemia. The alkaline phosphatase, when increased, showed a decrease to the normal range. A significant decrease in osteoclastic hyperactivity (active resorption surface, osteoclast index) and a slight increase in osteoblastic pool (active osteoid surface) were documented. No change was noted when osteomalacia predominated. Side effects included: anorexia, nausea, vomiting, face flushing. Our data suggest that salmon CT may be usefully employed in chronic uremic patients on RDT, when secondary hyperparathyroidism predominates.
Nephron 1979
PMID:Effect of calcitonin on bone lesions in chronic dialysis patients. 49 16

Three adolescents with uraemic osteodystrophy were treated for 7 months with daily oral doses of 1alpha-hydroxycholecalciferol (0.25-10.0 mug). All the patients were hypocalcaemic and had high serum levels of alkaline phosphatase before the treatment. A rapid rise in serum calcium and a slow, but pronounced decline in serum alkaline phosphatase concentration were observed during the period of treatment. 1alpha-Hydroxycholecalciferol induced hypercalcaemia in two situations. In both cases the hypercalcaemia was transient, serum calcium being normalized in a few days by withdrawal of the drug. Withdrawal of the drug also in other situations resulted in a fall in serum calcium concentration in a couple of days. This suggests that 1alpha-hydroxycholecalciferol should be given daily or every other day. The response did not subside during 7 months of treatment. On the contrary, the maintenance dose necessary to keep serum calcium constant was smaller than the initial dose necessary to normalize serum calcium. Bone mineral content, estimated by photon absorptiometry, rose. The rachitic bone lesions seen radiologically were significantly ameliorated during the treatment.
Nephron 1976
PMID:1alpha-hydroxycholecalciferol. Long-term treatment of patients with uraemic osteodystrophy. 126 9

Authors report on the effect of reduced glutathione parenterally administered on the anemic status in patients suffering from chronic renal failure and undergoing hemodialysis. Twenty patients were studied for 180 days and were divided into two age- and sex-matched groups. The first group (10 patients) received placebo, the second group (10 patients) received the treatment (1,200 mg of reduced glutathione). Reduced glutathione and placebo were given for 120 days in a randomized double-blind fashion and the following measurements were performed: red blood cells reduced and oxidized glutathione, plasma reduced and oxidized glutathione, hematocrit, hemoglobin, reticulocytes, serum iron, transferrin, indirect bilirubin, urea, creatinine, calcium, phosphate, parathyroid hormone and alkaline phosphatase. In the treated group, during the supplementation period, there was an increase in the levels of red blood cells and plasma reduced glutathione, hematocrit and hemoglobin and a concomitant decrease in plasma oxidized glutathione and reticulocytes with a maximum effect on the 120th day of therapy. In the placebo-treated group there were no significant variations of the parameters considered during the study period. When the therapy, on patients undergoing treatment, was terminated there was a drop in the analyzed parameters, which fell to pretreatment values at the subsequent controls. These findings seem to indicate that reduced glutathione could represent a useful drug in the treatment and management of anemia in patients affected by chronic renal failure.
Nephron 1992
PMID:Anemia and chronic renal failure: a therapeutical approach by reduced glutathione parenteral administration. 150 36

Parameters of calcium and phosphate metabolism were measured in 27 patients with mild renal failure [glomerular filtration rate (GFR) 40-90 ml/min], 12 patients with moderate renal failure (GFR 20-39 ml/min) and in 12 healthy subjects. GFR was determined by technetium-99m diethylenetriamine penta-acetic acid clearance. Intact parathyroid hormone (PTH) was measured by a sensitive immunochemiluminometric assay and somatomedin-C was determined by radioimmunoassay. Both 1,25-dihydroxyvitamin D [1,25(OH)2D] and vitamin-D-binding protein were measured allowing calculation of the free 1,25(OH)2D index. By linear regression and multivariate analysis, PTH was negatively and independently correlated with GFR, plasma bicarbonate and 25-hydroxyvitamin D [25(OH)D] while free 1,25(OH)2D was positively correlated with GFR. Increased PTH secretion and reductions in 1,25(OH)2D were present in mild renal failure patients before any changes in plasma calcium, phosphate and bicarbonate were noted. Plasma alkaline phosphatase was significantly higher in mild chronic renal failure patients compared to normal subjects, possibly indicating early effects of the secondary hyperparathyroidism on the skeleton. Somatomedin-C did not correlate with the free 1,25(OH)2D index or a measure of 1,25(OH)2D production. It is concluded that the secondary hyperparathyroidism which occurs very early in the onset of chronic renal failure may be due to a reduction in the circulating concentration of 1,25(OH)2D consequent upon the renal failure. Low plasma bicarbonate and 25(OH)D also appear to be determinants of a raised PTH concentration. The compensatory increase in PTH presumably maintains extracellular calcium and phosphate levels constant but with possible deleterious effects on the skeleton.
Nephron 1992
PMID:Determinants of intact parathyroid hormone and free 1,25-dihydroxyvitamin D levels in mild and moderate renal failure. 150 39

The purpose of this study is to evaluate the place of intravenous 1 alpha-hydroxyvitamin D3 (1 alpha-OH-D3) in the prevention of radiologically obvious hyperparathyroidism (HPT) in patients on maintenance dialysis while excluding aluminium phosphate binder and using a dialysate calcium concentration of 1.62 mmol which keeps the intradialytic calcium balance neutral. Therefore, 47 patients without subperiosteal resorption and previously treated by oral CaCO3 and if necessary Mg(OH)2 as phosphate binder while their dialysate calcium had a Ca level of 1.62 and a Mg level of 0.2 mmol/l were randomized into a control group of 24 who were maintained on the same treatment and an experimental group of 23. This group discontinued CaCO3 and received intravenous 1 alpha-OH-D3 after each dialysis at increasing doses up to 4 micrograms and increased Mg(OH)2 as their sole phosphate binder. When plasma Ca increased above 2.7 mmol/l, the dose of 1 alpha-OH-D3 was decreased. When plasma PO4 increased above 2 mmol/l, the dose of Mg(OH)2 was increased to the highest dose not inducing diarrhea, hypermagnesemia (less than 2 mmol/l) or hyperkalemia (less than 6 mmol/l). In case of persistent hyperphosphatemia, the dose of 1 alpha-OH-D3 was decreased. Since mean plasma alkaline phosphatase was normal, HPT was monitored on the plasma concentration of 1-84 PTH for which a previous histological study showed that frank osteitis fibrosa was present only when they were above 70 pg/ml, i.e. (about twice the upper limit of the normal value). Before the study, plasma PTH was below this limit in 16 patients of the CaCO3 group and in 14 patients of the 1 alpha-OH-D3 group. After 6 months, they remained below this limit in all patients except 2 of each group. Plasma PTH was initially above 70 pg/ml in 8 of the CaCO3 and did not change significantly throughout the study, 2 patients having at 6 months a PTH level below 70 pg/ml. In contrast with intravenous 1 alpha-OH-D3, all the 9 patients with initial frank HPT decreased their PTH levels after 2 months, the levels being below 70 pg/ml in 6 cases. However, because of hypercalcemia and/or of hyperphosphatemia in spite of a highest tolerable dose of Mg(OH)2, 1 alpha-OH-D3 doses had to be decreased down to 0.4 microgram per dialysis at the 6th month so that at 6 months 6 of 9 patients had their PTH levels above 70 pg/ml, a number comparable to that of patients treated with CaCO3 (6 of 8).(ABSTRACT TRUNCATED AT 400 WORDS)
Nephron 1992
PMID:Prevention of hyperparathyroidism in patients on maintenance dialysis by intravenous 1-alpha-hydroxyvitamin D3 in association with Mg(OH)2 as sole phosphate binder. A randomized comparative study with the association CaCO3 +/- Mg(OH)2. 155 99

Uremic patients may develop extraskeletal calcifications. Among the latter, periarticular tumoral calcifications (TC) represent massive, multiloculated calcium-phosphate deposits. The aim of this report was to analyze a series of 10 cases of TC in hemodialysis patients who were admitted at the Necker Hospital between 1974 and 1988. They were all male. An increased plasma calcium x phosphorus product was observed in 8 of the 10 patients. Plasma calcium level was increased in only 2 patients. In contrast, hyperphosphatemia was a constant feature in all the patients, as was the absence of an increase in plasma alkaline phosphatase activity. Using the bone histomorphometry technique, osteitis fibrosa of mild degree was observed in 2 patients, of moderate degree in 2 and of severe degree in 2 others. Evidence of aluminum (Al) overload was found in the 8 patients in whom it was searched based on bone histomorphometry, bone histochemistry, bone Al content and increased serum Al levels either in the basal state or after a deferoxamine test. In addition, Al overload was strongly suspected in the 2 remaining patients because of prolonged exposure to Al-contaminated dialysate. Various treatment strategies, including parathyroidectomy (PTx), were undertaken that remained unsuccessful in modifying the course of TC to a significant extent. Remarkably, TC occurred for the first time after PTx in 1 patient and worsened after PTx in 2 others. In conclusion, overt secondary hyperparathyroidism appears not to be an essential prerequisite for TC development in hemodialysis patients, and PTx must not be performed in such patients on the sole basis of the presence of TC.(ABSTRACT TRUNCATED AT 250 WORDS)
Nephron 1992
PMID:Tumoral calcifications in hemodialysis patients: possible role of aluminum intoxication. 156 77

Many hemodialysis patients are still suffering from secondary hyperparathyroidism although 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) has been used to treat renal osteodystrophy for the last two decades. The main reason for its failure to correct the secondary hyperparathyroidism is that in patients, hypercalcemia occurs before adequate parathyroid hormone (PTH) suppression is obtained when a large daily dose of 1,25(OH)2D3 is started. In this study, the oral dose of 1,25(OH)2D3 (4.0 micrograms) was administered only twice a week at the end of hemodialysis ('oral 1,25(OH)2D3 pulse therapy'), in 19 patients with severe secondary hyperparathyroidism. Serum immunoreactive PTH started to decrease after 6 weeks of therapy, and the original level of 41.2 +/- 7.24 was reduced to 24.4 +/- 6.12 ng/ml by the end of the 6-month therapy (p less than 0.001). Serum alkaline phosphatase also was reduced by 64.4%. Three out of 19 patients suffered from hypercalcemia during the 4th month of therapy. Calcium supplement given to 6 other patients with severe secondary hyperparathyroidism did not lower serum PTH levels significantly after 6 weeks of therapy, although serum calcium levels increased and were sustained above 10 mg/dl for the last 5 weeks. These findings strongly suggest that the suppressive effect of the oral 1,25(OH)2D3 pulse therapy was attained by a direct action of 1,25(OH)2D3 on the parathyroid gland rather than by its ability to elevate serum calcium levels. In conclusion, the oral 1,25(OH)2D3 pulse therapy effectively lowered PTH levels in hemodialysis patients who cannot tolerate large daily doses of 1,25(OH)2D3.
Nephron 1991
PMID:The 'oral 1,25-dihydroxyvitamin D3 pulse therapy' in hemodialysis patients with severe secondary hyperparathyroidism. 204 11

To evaluate the relationship between hyperparathyroid bone X-ray lesion, biochemical parameters and bone histology in chronic renal failure, 59 patients (52 +/- 14.9 years; Crs 4.7 +/- 2.2 mg/dl, mean +/- SD) on conservative treatment and 103 (48 +/- 14 years) on hemodialysis (from 48.4 +/- 36.7 months) were studied. Right-hand X-ray was carried out for evaluation of the scores (0-3) of acroosteolysis (score A) and subperiosteal resorption (score B). Serum iPTH, osteocalcin and alkaline phosphatase (AP) were measured. In addition in a subset of 53 patients, 30 in predialysis and 23 in dialysis, a bone biopsy was performed for histomorphometry. In predialysis the scores A and B correlated with bone GLA protein (BGP) (p less than 0.01), AP (p less than 0.05) and osteoid surface (p less than 0.05) and 0.01 respectively). In hemodialysis the same level of significant correlation (p less than 0.001) was found between the scores and the three humoral parameters. Score A correlated with active osteoblastic surface and active resorption surface while score B correlated with active osteoblastic surface (p less than 0.01), osteoid surface and active resorption surface (p less than 0.05). Multiple regression analysis carried out to establish the predictive variables of bone histologic lesions (active resorption surface and active osteoblastic surface) singled out BGP in predialysis and AP and the two scores in dialysis. We conclude that serum BGP, as compared to PTH and AP, prevails as a valid marker of hyperparathyroid bone lesion in predialysis, while in dialysis it does not seem to add further information to that carried by other variables.(ABSTRACT TRUNCATED AT 250 WORDS)
Nephron 1990
PMID:Osteocalcin, iPTH, alkaline phosphatase and hand X-ray scores as predictive indices of histomorphometric parameters in renal osteodystrophy. 207 8


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