hyperphosphatemia/phosphatase

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Hyperphosphatemia, Phosphoprotein Phosphatases, and Microparticle Release in Vascular Endothelial Cells.

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Hyperphosphatemia in patients with advanced CKD is thought to be an important contributor to cardiovascular risk, in part because of endothelial cell (EC) dysfunction induced by inorganic phosphate (Pi). Such patients also have an elevated circulating concentration of procoagulant endothelial

[Electrophoresis of alkaline phosphatase isoenzymes--the key to rapid diagnosis in transient hyperphosphatemia].

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Using the method of electrophoretic separation of isoenzymes of serum alkaline phosphatase the authors confirmed the diagnosis of transient hyperphosphatasaemia in nine children examined in the out-patient department or hospitalized with various diagnoses in the Childrens Hospital. The typical

Tumoral calcinosis with hyperphosphatemia.

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Tumoral calcinosis is a rare disorder of mineral metabolism among adolescents and young adults characterized by deposition of calcific masses around large joints. It is less commonly reported in pediatric population and commonly mistaken for bone tumors. Typical lab parameters include

Calcifying human aortic smooth muscle cells express different bone alkaline phosphatase isoforms, including the novel B1x isoform.

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BACKGROUND Vascular calcification, causing cardiovascular morbidity and mortality, is associated with hyperphosphatemia in chronic kidney disease (CKD). In vitro, phosphate induces transdifferentiation of vascular smooth muscle cells to osteoblast-like cells that express alkaline phosphatase (ALP).

[Hypercalcemia and hyperphosphatemia in thyrotoxoicosis and the therapeutic effect of propranolol].

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Measured levels of serum calcium, phosphate, alkaline phosphatase, and urinary hydroxyproline were measured and calcium-phosphate product was calculated in 20 hyperthyroid patients and 20 normal controls. Eleven of the patients took propranolol 160 mg per day for 28 days. We found that the serum

A Role of Intestinal Alkaline Phosphatase 3 (Akp3) in Inorganic Phosphate Homeostasis.

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OBJECTIVE Hyperphosphatemia is a serious complication of late-stage chronic kidney disease (CKD). Intestinal inorganic phosphate (Pi) handling plays an important role in Pi homeostasis in CKD. We investigated whether intestinal alkaline phosphatase 3 (Akp3), the enzyme that hydrolyzes dietary Pi

[Alkaline phosphatase isoenzyme activity in the serum of women during the second half of pregnancy].

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The authors determined total alkaline phosphatase activity as well as the activity of placental, bone marrow and liver isoenzymes in sera of 185 pregnant women with normal pregnancy, divided, into 6 groups according to their gestational age (from 20 to 40 weeks' gestation). It was established an

Combined alkaline phosphatase and phosphorus levels as a predictor of mortality in maintenance hemodialysis patients.

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Hyperphosphatemia-induced vascular calcification and higher alkaline phosphatase (ALP) levels-related high-turnover bone diseases are linked to mortality among patients with chronic kidney disease (CKD). Nonetheless, no large epidemiological study in patients with CKD has been conducted to

Increases of serum phosphorus concentration and duodenal, renal and femur alkaline phosphatase (EC 3.1.3.1) activities of normal rats fed 2000 ppm aluminum diets.

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In order to investigate the dietary effect of calcium on aluminum-induced hypophosphatemia, five types of diet, sucrose, lactose, milk, casein and soy protein, were prepared. These diets differed with regard to Ca concentration, and carbohydrate or protein sources which were expected to modify

Hypophosphatasia: the importance of alkaline phosphatase in bone mineralization.

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The authors describe a neonate who was diagnosed with "perinatal hypophosphatasia". The clinical manifestations in this patient were small head size, soft calvarium (caput membranaceum), and short bowing forearms and legs. Laboratory investigations revealed hypercalcemia at 12.7 mg/dl,

Hyperphosphatemia in infantile hypophosphatasia: implications for carrier diagnosis and screening.

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Twenty obligate carriers of infantile hypophosphatasia (HOPS), a severe autosomal recessive metabolic bone disorder, were studied and compared with 36 controls. Decreased serum alkaline phosphatase activity and increased urinary phosphoethanolamine excretion were confirmed in the HOPS carriers.

Control of predialytic hyperphosphatemia by oral calcium acetate and calcium carbonate. Comparable efficacy for half the dose of elemental calcium given as acetate without lower incidence of hypercalcemia.

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Since Mai et al. found, with the intestinal lavage technique, that the same dose of elemental calcium given as acetate (Ca Ac) complexed in the gut of uremic patients twice as much phosphate as calcium carbonate (CaCO3) while inducing a rather low calcium absorption, we wanted to see if half the

Efficacy of hyperphosphatemia control in the progression of chronic renal failure and the prevalence of cardiovascular calcification.

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OBJECTIVE Chronic kidney disease mineral- and bone disorder (CKD-MBD) has been studied more often in dialysis than in predialysis CKD patients. The association between efficacy of hyperphosphatemia control and chronic renal failure (CRF) progression, prevalence of bone disease and cardiovascular

Plasma bone-specific alkaline phosphatase changes in hemodialysis patients treated by alfacalcidol.

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Vitamin D derivatives correct high bone remodeling by decreasing plasma iPTH concentration in uremic patients with secondary hyperparathyroidism. However, without bone biopsy, plasma iPTH alone might not provide sufficient information regarding vitamin D-induced bone changes. Plasma bone-specific

Sevelamer hydrochloride improves hyperphosphatemia in hemodialysis patients with low bone turnover rate and low intact parathyroid hormone levels.

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Sevelamer improves hyperphosphatemia without increasing the calcium load. However, it remains unknown whether sevelamer restores bone metabolism in hemodialysis patients with low bone turnover osteodystrophy and hypoparathyroidism. We investigated the changes in serum intact parathyroid hormone

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