hyperphosphatemia/carbohydrate

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Hyperphosphatemia

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Phosphate is an abundant mineral found in the body. The body store of phosphate is 500 to 800 g, with 85% of the total body phosphate present in crystals of hydroxyapatite in the bone — about 10% found in muscles and bones in association with proteins, carbohydrates, and lipids. The rest gets

Endocrine crises. Hypophosphatemia and hyperphosphatemia.

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Pathophysiology, clinical sequelae, and treatment for hypophosphatemia and hyperphosphatemia are discussed. Hypophosphatemia results from a variety of conditions including malnutrition, carbohydrate refeeding, acid-base disorders, and hormonal and drug effects. Patients suffering from severe

Practical approaches to management of hyperphosphatemia: can we improve the current situation?

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Despite advanced technology and regular and efficient dialysis treatment, the prevalence of hyperphosphatemia still is unacceptably high. Nevertheless, a neutral phosphorus balance level can generally be achieved by optimization of dialysis prescription in combination with individualized dietary and

Management of hyperphosphatemia.

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Hyperphosphatemia is a well recognized risk factor for cardiovascular mortality in dialysis patients. Despite advanced technology and regular and efficient dialysis treatment the prevalence of hyperphosphatemia is still high. The goal of normalization of serum phosphorus (iP) levels can only be

Chronic toxicity of propoxur on carbohydrate, protein and serum electrolyte levels in catfish, Heteropneustes fossilis.

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Alterations in the biochemical parameters of the catfish treated with low sublethal concentration (2.15 mg.L-1; 1/3 of 96 h LC50) of a carbamate pesticide-propoxur under static laboratory conditions for 10, 20 and 30 days were assayed. The fish elicited consistent hyperglycemia, concomitant with

Importance of plasma phosphate determination.

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Phosphate is an important component of all tissues and disorders of phosphate homeostasis are common in hospital populations. Hypophosphatemia, which is much more frequent than hyperphosphatemia, is commonly caused by infusion of carbohydrate or respiratory alkalosis. If hypophosphatemia is

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

Nutritional status and the role of diabetes mellitus in hemodialysis patients.

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This study was aimed to investigate the nutritional status and the role of diabetes mellitus in hemodialysis (HD) patients. Anthropometric, biochemical, and dietary assessments for HD 110 patients (46 males and 64 females) were conducted. Mean body mass index (BMI) was 22.1 kg/m(2) and prevalence of

The medical and metabolic consequences of administration of sodium acetate.

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1. The standard total parenteral nutrition, peritoneal dialysis, hemodialysis and many surgical fluids in use today contain 36 to 45 mM D,L-lactate or 2 to 140 mM acetate whereas the normal blood level of D-lactate is 0.02 mM L-lactate 0.5 to 5 mM and acetate 0.1 nM. The reasons for the continued

Nutritional status among peritoneal dialysis patients after oral supplement with ONCE dialyze formula.

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BACKGROUND Malnutrition is an important problem in patients treated with long-term dialysis, and most dialysis patients have lower dietary energy and protein intake. This study was undertaken to examine whether orally administered Otsuka Nutrition Pharmaceutical (ONCE) dialyze formula (ODF)

Ablation of vitamin D signaling rescues bone, mineral, and glucose homeostasis in Fgf-23 deficient mice.

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To explore further the role of the vitamin D axis for fibroblast growth factor-23 (FGF23) signaling, we mated Fgf-23 deficient (Fgf-23(-/-)) mice and vitamin D receptor (VDR) mutant mice with a non-functioning VDR. To prevent secondary hyperparathyroidism in VDR and compound mutant mice, all mice

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