Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

The examination of five pediatric patients with encephalopathy secondary to chronic renal failure has indicated a stereotyped sequence of neurologic signs and symptoms including ataxia, loss of motor abilities, myoclonus, seizures, dementia, and bulbar dysfunction. Both the patients with CNS dysfunction and a control group selected for a similar degree of renal failure had increased levels of serum phosphate, alkaline phosphatase, and parathyroid hormone. Serial EEGs in the affected group revealed progressive slowing and an increase in paroxysmal features. No specific neuropathologic findings were noted in one patient.
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PMID:Encephalopathy in infants and children with chronic renal disease. 729 12

The effects of 24,25-dihydroxyvitamin D3 (24,25[OH]2D3), given orally for 7-10 days at doses of 2 and 4 microgram/day, were evaluated in patients with advanced renal failure. There was a significant fall in serum Ca and a rise in alkaline phosphatase; both returned to pretreatment levels 2 weeks after cessation of therapy. There was no change in intestinal absorption of 47Ca. These observations are significantly different from those observed during treatment with 1,25(OH)2D3 or 25(OH)D3, indicating that different vitamin D sterols can clearly exert different biologic effects.
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PMID:Unique effects of 24,25-dihydroxyvitamin D3 in uremic patients. 735 77

Alkaline phosphatase bone isoenzyme activity in serum correlates significantly to micromorphometrically assessed parameters of bone apposition as well as resorption. Though as both processes appear to be coupled in renal osteopathy, bone isoenzyme activity seems to reflect mainly hyperosteoid states. The detection of abnormal findings is impressively better by bone isoenzyme analysis as compared with total alkaline phosphatase activity; pathological values are found even at the initial phase of osteopathy in early renal failure. The determination of alkaline phosphatase bone isoenzyme activity in serum is a sensitive and reliable diagnostic tool in assessing the beginning and degree of metabolic bone disease.
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PMID:Alkaline phosphatase bone isoenzyme activity in serum in various degrees of micromorphometrically assessed renal osteopathy. 740 46

Although disorders of renal calcitriol synthesis play an important role in the pathogenesis of secondary hyperparathyroidism in the early and moderate phase of chronic renal failure, the treatment of secondary hyperparathyroidism with vitamin D metabolite has not attained consensus from the view point that is accelerates the progression of renal disease. The aim of this study was to evaluate the efficacy and adverse effect of low-dose daily oral treatment of 1.25 vitamin D for patients with mild to moderate renal failure. Fifteen chronic renal failure patients with serum creatinine ranging from 2.5 to 6.1 mg/dl and serum intact parathyroid hormone ranging from 100 to 450 pg/ml, were treated with oral 0.25-0.5 micrograms of 1.25 vitamin D for six months, after a six month control periods. In the six months control periods, serum intact parathyroid hormone, alkaline phosphatase activity, and bone gla protein increased significantly, however after the treatment of 1.25 vitamin D, serum intact parathyroid hormone, alkaline phosphatase activity, and bone gla protein decreased significantly. Serum calcium concentration increased significantly after the initiation of 1.25 vitamin D treatment, so it could not be ascertained whether or not 1.25 vitamin D directly suppressed parathyroid hormone synthesis. Bone mineral densities did not change within one year. Renal function was evaluated from the slopes of the reciprocal serum creatinine concentration versus time. The slopes did not change after the administration of 1.25 vitamin D. In conclusion, 1.25 vitamin D treatment of secondary hyperparathyroidism in patients with mild to moderate renal failure had beneficial therapeutic effect on humoral bone parameters, and did not show any adverse effect on renal function.
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PMID:[Treatment of secondary hyperparathyroidisms of predialysis chronic renal failure with low doses of 1.25(OH)2D3]. 747 6

In this study, we compared results obtained in protein calorie malnourished (PCM) monkeys and controls given Cd2+ (5 mg Cd2+/kg body wt./day) orally for 24 weeks. After 16 weeks of Cd2+ exposure, an indolent renal failure develops in PCM monkeys which resulted in significant increase in urinary excretion of total protein, Cd2+, Zn2+ and Ca2+ as compared to corresponding to Cd(2+)-treated control group. In isolated proximal tubule brush border membrane vesicles (BBMV), Cd2+, Zn2+ and Ca2+ transport were significantly impaired in Cd(2+)-exposed PCM monkeys as compared to Cd(2+)-treated controls. The mechanism of higher urinary excretion of Cd2+, Zn2+ and Ca2+ was examined by analyzing the kinetic parameters of transport systems. The kinetic studies of Cd2+, Zn2+ and Ca2+ transport systems in the BBMV preparations of Cd(2+)-exposed PCM monkeys exhibited a significant decrease in Vmax and an appreciable increase in Km as compared to Cd(2+)-treated controls. These findings suggested that Cd2+ treatment of PCM monkeys caused either a decrease in the number of transporters in the brush border membrane or an increase in the number of less active transporters for Cd2+, Zn2+ and Ca2+. Furthermore, brush border membrane-bound enzymes, viz. alkaline phosphatase and leucine aminopeptidase, activities were significantly impaired in Cd(2+)-exposed PCM monkeys. Cadmium content in kidney cortex of Cd(2+)-exposed PCM monkeys was 3.34-fold higher than Cd(2+)-exposed controls. These findings also established that Cd2+ not bound to metallothionein (MT) was significantly higher in Cd-exposed PCM monkeys, which may be an important determinant in renal toxicity by interacting with sensitive sites in the renal cells and causing renal damage in Cd-exposed PCM monkeys.
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PMID:Cadmium-induced nephrotoxicity in rhesus monkeys (Macaca mulatta) in relation to protein calorie malnutrition. 762 86

The present study was performed to measure the uptake of main renal cortical fuel substrates (glutamine and lactate) and the release of the main renal cortical products (ammonia and glucose) by cortical slices from gentamicin-treated rats. Experiments were done in 2 groups of female Wistar rats (250 g): In gentamicin group (n = 13), rats were injected s.c. with gentamicin-sulphate 100 mg/Kg body wt/day for 5 days. Control rats (n = 13) received isotonic saline. After anesthesia and blood sampling, renal cortical slices were obtained and incubated with L-glutamine and/or lactate at 1 or 5 mM concentration, containing L-glutamate and/or pyruvate at 0.1 or 0.5 mM. Creatinine clearance was reduced to a 50% in gentamicin-treated rats. In addition these animals showed a sharp increase in urinary excretion of N-acetyl-beta-D-glucosaminidase and alkaline phosphatase. Light microscopy examination revealed extensive cell necrosis and tubular obstruction of the proximal tubules in kidneys of rats injected with gentamicin. The renal cortical gentamicin concentration of rats injected with gentamicin was 310 +/- 43 mu/g, whereas it was undetectable in control rats. Cortical slices from gentamicin-treated rats, compared to control ones, showed a reduced production of ammonia and glucose, without differences in glutamine or lactate extraction. These alterations can be explained by both the increased rate of anabolic reactions to recover cell damage associated to renal failure, as well as by a direct effect of gentamicin on the rate of carboxylation reactions.
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PMID:Effect of gentamicin treatment on glutamine and lactate metabolism by the renal cortex of the rat. 769 Dec 12

The bone histology of renal osteodystrophy is classified into osteitis fibrosa, osteomalacia, those of mixed, osteoporosis and low turnover bone. Osteitis fibrosa is the most frequent skeletal abnormality and is caused by various degrees of hyperparathyroidism. The main factors inducing hyperparathyroidism which is a well known complication in patients with renal failure include (a) phosphorus retention: 1) hypocalcemia and 2) decreased levels of 1 alpha, 25(OH)2 Vitamin D3, (b) reduced number of 1 alpha, 25(OH)2 Vitamin D3 receptors in parathyroid tissue, (c) skeletal resistance to set-point for calcium-regulated parathyroid hormone secretion. Serum or plasma levels of calcium, phosphorus, alkaline phosphatase, parathyroid hormone, calcitonin and tartrate resistant acid phosphatase are measured to evaluate hyperparathyroidism and metabolic bone disease. Dietary phosphorus restriction in chronic renal insufficiency prevents secondary hyperparathyroidism and renal osteodystrophy. Other treatment of phosphorus binders, Vitamin D metabolites or analogues, carcitonin and bisphosphonate are useful for the management of renal bone disease.
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PMID:[Secondary hyperparathyroidism and tertiary hyperparathyroidism chronic renal failure, uremia]. 775 92

Agarose electrophoresis (Isopal, Beckman) and an immunoradiometric assay (IRMA) involving specific monoclonal antibodies (Ostase, Hybritech), two methods for the quantification of serum bone alkaline phosphatase (ALP, EC 3.1.3.1), a marker of osteoblastic activity, were compared in 293 patients: 79 with end-stage renal failure treated with hemodialysis and 214 with malignant disease. Overall correlation between the two methods was good (r = 0.92), except (a) for low values of bone ALP and (b) in some samples with high total liver ALP activity--both due to considerable cross-reactivity of the anti-bone ALP antibodies of the Ostase kit with liver ALP. This interference was not constant and was not evenly distributed across all concentrations of bone ALP. Low bone ALP determined with the IRMA (< or = 5 micrograms/L) was confirmed by electrophoresis (< or = 21 U/L), but bone ALP activity determined by electrophoresis to be low (< or = 21 U/L) was not correlated with the IRMA results. After standardizing our results by computing z-values for bone ALP, delta z (= zOstase - zIsopal) was significantly correlated with liver ALP activity (r = 0.73, P < 0.0001). We conclude that the IRMA for quantifying bone ALP is acceptable as a screening method. However, when high values for bone ALP are found with the Ostase method, confirmation by electrophoresis remains mandatory to rule out cross-reactivity with high amounts of liver ALP. For detecting low bone ALP activities, electrophoresis remains the method of choice.
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PMID:Immunoradiometric method and electrophoretic system compared for quantifying bone alkaline phosphatase in serum. 776 3

We administered calcium carbonate orally to determine its safety and efficacy in treating nondialyzed patients with mild to moderate renal failure and secondary hyperparathyroidism. Twenty patients with chronic renal failure (creatinine clearance levels ranging from 7.9 to 42.7 mL/min) participated in this study. After a 6-month control period, 3 g calcium carbonate was administered daily for 6 months. We studied the effect for another 6 months after discontinuation of the regimen. We found that serum-intact parathyroid hormone was suppressed from 183 +/- 149 pg/mL to 85 +/- 61 pg/mL (P < 0.05) by treatment. This suppression was achieved with no increase in serum concentrations of 1,25(OH)2D3. Serum phosphorus levels decreased from 3.4 +/- 0.7 to 3.0 +/- 0.7 mg/dL (P < 0.01) and Ca2+ concentration increased significantly from 2.40 +/- 0.12 mEq/L to 2.57 +/- 0.08 mEq/L (P < 0.001) at 6 months. These changes were reversed after the 6-month period of withdrawal from calcium carbonate. Deterioration of renal function was not exacerbated by the therapy. Calcium carbonate administration also suppressed the serum concentrations of alkaline phosphatase and osteocalcin, indicating that improvement of hyperparathyroid bone disease is possible without a vitamin D3 supplement at an earlier stage of renal failure. Thus, administration of 3 g oral calcium carbonate daily was highly effective in treating secondary hyperparathyroidism in patients with mild to moderate renal failure.
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PMID:Effect of administering calcium carbonate to treat secondary hyperparathyroidism in nondialyzed patients with chronic renal failure. 777 84

We studied the relationship between the histomorphometric parameters of bone structure in biopsied iliac crest bone specimens and the serum biochemical parameters in 62 chronic renal failure (CRF) patients at the time of starting hemodialysis. These patients were classified into 4 groups according to Coburn's definition: 4 patients with osteomalacia, 1 with osteitis fibrosa, and 57 with mild type. Serum corrected Ca levels were significantly lower in cases with osteomalacia than those of mild type, which suggested that hypocalcemia was related to Calcification disturbance in end-stage renal failure. The bone histomorphometry revealed that in CRF patients, osteoid and bone resorption parameters were significantly higher and calcification parameters were significantly lower than those of normal controls. Osteoclast and osteoblast surfaces were significantly correlated with osteoid and bone formation parameters. In diabetic nephropathy patients, serum C-PTH levels were significantly lower than those of patients with non-diabetic nephropathies. Bone mass, osteoid and bone formation parameters were also significantly lower in diabetic nephropathy patients, which showed that low turnover bone mass decrement has already appeared at the time of starting hemodialysis. There was a significant negative correlation between serum corrected Ca levels and osteoid parameters. A significant relationship was also found between serum alkaline phosphatase levels and both osteoid and bone formation parameters. Serum C-PTH levels were significantly related to osteoid, bone resorption and bone formation parameters, demonstrating the presence of high turnover bone in secondary hyperparathyroidism. This study clarifies that morphological changes of bone structure are present at the time of starting hemodialysis in CRF patients.
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PMID:[Studies on the pathogenesis and pathophysiology of renal osteodystrophy. II. Bone histology of chronic renal failure patients at the time of starting hemodialysis]. 781 47


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