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)

Hyperparathyroid bone disease is a common complication of end stage renal failure, particularly in patients on maintenance haemodialysis. Several studies have, however, shown a near absence of hyperparathyroid bone disease in diabetic patients who have been receiving haemodialysis for periods of up to 4 years. We have studied biochemical indices of mineral metabolism in 54 consecutive pre-dialysis patients with moderate to severe renal impairment. Deteriorating renal function was associated with developing hypocalcaemia and hyperphosphataemia. Hypocalcaemia was strongly related to increased severe alkaline phosphatase activity (p less than 0.001), suggesting the development of hyperparathyroidism. Five patients with hypocalcaemia and increased alkaline phosphatase were studied in detail. All had elevated serum concentrations of parathyroid hormone and histological signs of hyperparathyroidism on bone biopsy. Three of the patients had low serum 25 hydroxyvitamin D levels with associated osteomalacia, the other 2 patients were notable for their long duration of renal failure. In the long-term (greater than 4 years) we also observed the development of hyperparathyroidism in a small group of diabetic patients maintained on haemodialysis. We conclude that diabetic patients are not uniquely protected against renal osteodystrophy. Although the prevalence of hyperparathyroidism may be lower in diabetic patients than in those with other types of renal disease, the same factors which predispose to bone disease in non-diabetic patients (long duration of renal failure, low serum 25 hydroxyvitamin D and long periods on haemodialysis) also operate in the diabetic population.
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PMID:Hyperparathyroid bone disease in diabetic renal failure. 213 93

Renal osteodystrophy is multifactorial. Decreased calcium absorption from the GI tract, secondary to low calcitriol levels; hyperphosphatemia; skeletal resistance to the action of parathormone; and aluminum deposition on the surface of the bones are its main pathogenetic mechanisms. Its biochemical features include abnormalities in serum calcium, phosphate, alkaline phosphatase, parathormone, calcitriol, and aluminum concentration. Radiographic methods are of little use in the characterization of the type of osteodystrophy present, but they may be of help in assessing mineral loss from the skeleton. Clinical manifestations are from bones (pain, deformities, fractures) or from metastatic calcifications. Bone biopsy is the definitive means of diagnosis. The main histologic types of osteodystrophy include osteitis fibrosa, osteomalacia, mixed form (with features of both osteitis fibrosa and osteomalacia), and aluminum osteodystrophy (presenting as either osteomalacia or aplastic lesion). The management of renal osteodystrophy should address all the pathogenetic mechanisms. Correction of the abnormalities in calcium and phosphate metabolism and prevention of aluminum osteodystrophy are the cardinal rules of management. Specific measures (parathyroidectomy, chelation of aluminum) have clear-cut indications and usually require a bone biopsy.
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PMID:Diagnosis and management of bone disorders in chronic renal failure and dialyzed patients. 219 65

Since 1980, moderately large doses of oral calcium (80 +/- 35 mmol/day as CaCO3 +/- calcium polystyrene sulphonate), in association if necessary with Mg(OH)2 (2.5 +/- 1 g/day), with a reduction in the dialysate Mg concentrations from 0.75 to 0.375 mmol/24 h, have replaced A1(OH)3 as phosphate binders in our centre. A1(OH)3 was previously given to our haemodialysis patients in association with small doses of Ca CO3 (less than or equal to 3 g/day) and if necessary with 1 alpha OH vitamin D3. To compare the long-term efficacy of this new approach with the former one in the prevention of renal osteodystrophy and soft-tissue calcification, 32 current patients were selected on the basis of at least 24 months of treatment in our centre and availability of a yearly bone survey (profile of lumbar spine and anteroposterior view of the pelvis, shoulders and hands). A group of 30 patients treated before 1980 were then selected on the same criteria and matched for age, sex, and duration on dialysis. Linear calcifications of the anterior and posterior walls of the aorta in front of L2, L3, L4 and on the lateral walls of the iliac and femoral arteries were measured and the para-articular calcifications and subperiosteal resorptions of the hands evaluated. The initial extent and the subsequent increase of the ocular and para-articular calcification were comparable in the two groups. Plasma alkaline phosphatase was stable in the normal range in both groups, as was plasma concentration of calcium. Plasma phosphate was slightly elevated (1.7 mmol/l) but stable and comparable in the two groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Prevention of osteitis fibrosa, aluminium bone disease and soft-tissue calcification in dialysis patients: a long-term comparison of moderate doses of oral calcium +/- Mg(OH)2 vs Al(OH)3 +/- 1 alpha OH vitamin D3. 251 25

Osteocalcin serum levels reflect bone turnover. In renal insufficiency secondary hyperparathyroidism and reduced renal clearance might be responsible for elevated serum levels of osteocalcin. Renal transplantation might improve renal osteodystrophy and therefore could influence osteocalcin serum levels. We determined the influence of renal transplantation on osteocalcin levels in 37 consecutive patients (25m/12f) by RIA. Blood samples were collected prior to, 3 days, 28 days, 6 months and 12 months after renal transplantation. Prior to renal transplantation osteocalcin levels were significantly elevated (mean +/- s: 23.4 +/- 12.8 ng/ml) compared to healthy volunteers (4.1 +/- 1.4 ng/ml). Following renal transplantation osteocalcin decreased significantly (9.4 +/- 8.9 ng ml) 3 days and (7.1 +/- 7.8 ng/ml) 28 days. However, 6 and 12 months following renal transplantation the mean osteocalcin level increased again (8.3 +/- 5.7 ng/ml, 12.1 +/- 15.4 ng/ml). At 6 months 11 and at 12 months only 6 of 37 patients had osteocalcin levels in the normal range. 12 months following renal transplantation 21 out of 37 patients with elevated osteocalcin levels had parathyroid hormone levels above the normal range. Additionally to increased osteocalcin levels patients prior to renal transplantation had elevated alkaline phosphatase. Alkaline phosphatase had following renal transplantation a similar pattern as osteocalcin with initial decrease and secondary increase 6 and 12 months after renal transplantation. Parathyroid hormone was elevated in all patients before renal transplantation. Following renal transplantation mean parathyroid hormone levels tell significantly, however remained above normal range in 57% of these 37 patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Osteocalcin serum levels in patients following renal transplantation. 265 90

All patients with chronic renal failure have secondary hyperparathyroidism shown by elevated serum parathormone. Medical and surgical treatment is involves the use of phosphate binders, one alpha and increased frequency of dialysis. Surgery is indicated when medical treatment fails to control the Ca2+ PO4(2-) levels that activate renal osteodystrophy. High alkaline phosphatase and Ca2+ above 2.7 mmol/l are indications for surgery. Careful preoperative preparation and postoperative control minimise complications of haemorrhage, sepsis, tetany and cardiac arrhythmias. Long-term complications are hypoparathyroidism and recurrent hyperparathyroidism. Shortened dialysis periods may lead to increased parathyroid complications.
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PMID:Surgical treatment of secondary and tertiary hyperparathyroidism. 267 38

Nineteen bone biopsies with the Jamshidi needle were performed in 18 patients with renal osteodystrophy. The procedure was performed in the office or at the bedside and was tolerated well by all patients. These biopsies, plus clinical and laboratory studies provided all the information necessary to make therapeutic decisions. For most clinical purposes, serum calcium, phosphate, and alkaline phosphatase, a parathyroid hormone assay, spine and hand roentgenograms, and tetracycline-labeled Jamshidi needle biopsy of the iliac crest are satisfactory for the evaluation of renal osteodystrophy.
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PMID:Diagnosis of renal osteodystrophy with the Jamshidi needle biopsy. 275 Jan 79

Osteocalcin (OC), also called Bone Gla Protein (BGP), is a bone matrix protein of 5800 MW synthesized by osteoblasts. Since OC is mainly metabolized in the kidney, its blood concentration is altered in renal failure. The relationship between OC and the calcium-phosphorus regulating hormones (parathyroid hormone, calcitonin) and the biochemical parameters of bone metabolism (serum calcium, serum phosphorus and serum alkaline phosphatase) was studied in 30 patients on chronic hemodialysis (mean age: 51 years; mean duration of dialysis treatment: 39 months). OC levels were significantly elevated in all patients on chronic hemodialysis (34.7 +/- 31.5 ng/ml) when compared to healthy subjects (6.25 +/- 1.39 ng/ml, p less than 0.001). In 2 patients the OC levels were excessively high (127.54 ng/ml; 148.02 ng/ml), which was associated with severe renal osteodystrophy due to secondary hyperparathyroidism. When divided into 2 groups in the patients with secondary hyperparathyroidism the mean OC value was markedly elevated (50.5 +/- 12.7 ng/ml) compared to the patients without secondary hyperparathyroidism (24.1 +/- 2.8 ng/ml) (p less than 0.05). 70 per cent of the patients on chronic hemodialysis with OC levels greater than 30 ng/ml showed moderate to severe scintigraphic findings of bone disease. In neither of the 2 groups could a correlation between OC and serum alkaline phosphatase be demonstrated. The results indicate, that OC levels could be useful additional parameter in hemodialyzed patients with secondary hyperparathyroidism and OC levels could reflect bone formation in these patients.
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PMID:[Osteocalcin in chronic hemodialysis patients as an additional parameter in the diagnosis of advanced secondary hyperparathyroidism]. 278 25

The clinical, biochemical, radiological and scintigraphical data related to renal osteodystrophy were followed in 18 patients on CAPD for 3 to 5 years. The majority maintained normal serum calcium, bicarbonate and alkaline phosphatase concentrations; serum phosphate concentration decreased after starting CAPD but remained somewhat elevated. Only half of the patients needed phosphate binders. Serum PTH concentrations fell in those with high values at the start and remained stable in most others. Serum aluminum concentrations never exceeded 50 micrograms/l while serum 25(OH)D3 levels remained low. Bone radiology and scintigraphy were characterized by their stability over time. We think that CAPD, with the addition of calcium carbonate, phosphate binders and vitamin D analogs can achieve good control of renal osteodystrophy. In addition, joint problems are not common in CAPD patients but we present evidence that they too are at risk of dialysis amyloidosis.
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PMID:[Bone and joint complications in patients treated with continuous ambulatory peritoneal dialysis (CAPD) for more than 3 years]. 281 91

Serum bone Gla-protein (S-BGP) and other serum biochemical parameters, including alkaline phosphatase (S-AP) and immunoreactive PTH (S-iPTH), were measured in 42 patients undergoing chronic hemodialysis. Each patient also had a tetracycline-labeled transiliac bone biopsy, allowing correlations between the biochemical and trabecular bone histomorphometric parameters, S-BGP was markedly increased [64.0 +/- 74.8 (+/- SD) vs. 6.2 +/- 2.2 ng/ml in normal subjects] significantly correlated with S-AP (r = 0.53) and S-iPTH (r = 0.55) levels. S-BGP was significantly higher in the 14 patients with high turnover renal osteodystrophy (HT-ROD; S-BGP, 138.5 +/- 90.8 ng/ml) than in the 28 patients with low turnover (LT-ROD; S-BGP, 26.8 +/- 14.8 ng/ml). S-BGP was significantly correlated with the cellular parameters of bone resorption and formation (r = 0.57-0.69) and with the dynamic parameters of bone formation (r = 0.62-0.82). The extent of stainable bone aluminum was significantly negatively correlated with S-BGP (r = -0.51) and serum iPTH (r = -0.33), but not with S-AP. S-BGP measurement allowed better discrimination between LT-ROD and HT-ROD groups than did S-AP measurement. However, in the patients with LT-ROD, S-BGP did not discriminate between patients with or without osteomalacia. We conclude that S-BGP is a valuable marker for evaluating bone remodeling and, more specifically, the bone formation rate at the tissue level in hemodialyzed patients.
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PMID:Serum bone Gla-protein in renal osteodystrophy: comparison with bone histomorphometry. 348 98

Elevated levels of aluminum and beta 2-microglobulin have been demonstrated in chronic dialysis patients. The role of aluminum in the pathogenesis of renal osteodystrophy has also been shown. We report on the effects of beta 2-microglobulin on calcification in vitro using osteoblastic cells, clone MC3T3-El. At concentrations comparable to those in plasma of chronic dialysis patients, both beta 2-microglobulin and aluminum suppressed calcification while collagen synthesis and alkaline phosphatase activity were maintained. These observations may be related to the impaired bone mineralization frequently observed in chronic dialysis patients.
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PMID:Inhibitory effects of beta 2-microglobulin on in vitro calcification of osteoblastic cells. 354 31


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