Mineral metabolism phosphate

In this chapter, after an overview of bone and mineral metabolism, we discuss the clinical chemistry of calcium, phosphate, and magnesium the hormones regulating these minerals the major disorders of bone and the clinical use of markers of bone formation and degradation. A goal of the chapter is to provide, in one place, a view of these highly interrelated topics. 

Laboratory findings in rickets and osteomalacia include an increased serum ALP, with other alterations in bone and mineral metabolism dependent on the cause and severity of the disorder. ALP is usually increased because of the increased osteoblastic activity associated with producing unmineralized osteoid. Calcium may be low-normal or low in vitamin D deficiency depending on the severity of the disease. Phosphate may be normal or low, but falls with the development of secondary hyperparathyroidism. The serum calcium and PTH concentrations are usually normal in renal tubular defects of phosphate transport. Vitamin D nutrition may be assessed by the determination of serum 25(OH)D. Renal phosphate defects can be best assessed by determination of the renal phosphate threshold. 

Derangements in mineral metabolism frequently lead to metastatic calcification of soft tissue. Bone-seeking radionuclides, such as "Relabeled phosphate preparations, are proving particularly useful in detecting extra-skeletal calcification in situations where roentgenographic demonstration is lacking.61... 

Acetylated adipate- and glycerol-crosslinked starch, administered at 62% in a cooked diet, was safe to experimental rats.2115 Such esters, as well as acetylated starch phosphates, influenced mineral metabolism to a certain extent in rats, but... 

As in the case with abnormalities of glucose and electrolyte metabolism, all of the above disorders of mineral metabolism can be avoided if the physician is fully aware of the specific mineral composition of the infusate and if a careful monitoring schedule for plasma total calcium, inorganic phosphate and magnesium is adhered to. 

Mineral metabolism Refeeding hypophosphatemia is a risk during parenteral nutrition. In 70 patients with refeeding hypophosphatemia who were matched with controls the independent susceptibility factors were significant malnutrition a dose of less than 12 mmol of total phosphate during the first day and an initial rate of infusion of more than 70% of calculated requirements [62. Increasing amounts of non-lipid phosphate in the first day s regimen were protective. 

Factors that can predispose patients to developing metabolic bone disease include deficiencies of phosphorus, calcium, and vitamin D vitamin D and/or aluminum toxicity amino acids and hypertonic dextrose infusions chronic metabolic acidosis corticosteroid therapy and lack of mobility.35,39 Calcium deficiency (due to decreased intake or increased urinary excretion) is one of the major causes of metabolic bone disease in patients receiving PN. Provide adequate calcium and phosphate with PN to improve bone mineralization and help to prevent metabolic bone disease. Administration of amino acids and chronic metabolic acidosis also appear to play an important role. Provide adequate amounts of acetate in PN admixtures to maintain acid-base balance. 

Hypercalcemia Carefully monitor standard hypercalcemia-related metabolic parameters, such as serum levels of calcium, phosphate, and magnesium, as well as serum creatinine. Do not use loop diuretics until the patient is adequately rehydrated use with caution in combination with zoledronic acid in order to avoid hypocalcemia. Use zoledronic acid with caution with other nephrotoxic drugs. Concomitant use with estrogen/hormone replacement therapy (alendronate) Two clinical studies have shown that the degree of suppression of bone turnover (as assessed by mineralizing surface) was significantly greater with the combination than with either component alone. 

It regulates calcium metabolism by increasing calcium and phosphate absorption from the intestinal tract and also mobilises minerals from the bone. 

Metabolism of Ca - and phosphate, bone mineralization, resorption of Ca und phosphate in the intestine... 

While the high proportion of the mineral calcium in dairy products has been hypothesized as the factor contributing to favorable metabolic outcomes (Zemel, 2001), several studies have identified more favorable health outcomes in intervention trials whereby calcium is administered in the form of dairy products in contrast to supplementation (Zemel, 2004, 2008). It may be that the calcium phosphate found in dairy products exerts a more significant weight loss effect as opposed to the calcium citrate or calcium carbonate utilized in supplements (Lorenzen et al., 2006). 

Phosphorus is abundant on Earth, both as an element (the llth-most abundant atom in Earth s crust) and as phosphate. Meteorites hold a variety of phosphate-containing minerals and some phosphide minerals.10 Scientists at the University of Arizona have recently suggested that Fe3P, the mineral schreibersite, leads to the formation of phosphate and phosphite when corroded in water. Although phosphorylation of alcohols was not demonstrated, mechanistic considerations suggest that it should be possible. It is noteworthy that a clear prebiotic pathway for the chemical incorporation of phosphate into RNA or DNA has not been found. No nucleosides (nucleobases joined to sugars) have been reported from meteorites. Nor has evidence been found in any meteorite of the presence of nucleosides or nucleotides (nucleosides attached to phosphates). That suggests that nucleic acids were first formed as products of metabolism. 

Mineral nutrient limitation of microbial degradation has been put forward as an explanation for accumulation of carbon-rich DOM after a Phae-ocystis bloom (Thingstad and Billen 1994). The increase in carbohydrate/POC due to overflow metabolism will give rise to a substrate with a C/P and C/N ratio that is unfavorable to bacteria. Since the C/P ratio of bacteria may be considerably lower than that of phytoplankton (Vadstein et al. 1988), especially phosphate limitation may hamper microbial degradation (Thingstad et al. 

Vitamin D hormone is derived from vitamin D (cholecalciferol). Vitamin D can also be produced in the body it is formed in the skin from dehydrocholesterol during irradiation with UV light. When there is lack of solar radiation, dietary intake becomes essential, cod liver oil being a rich source. Metabolically active vitamin D hormone results from two successive hydroxylations in the liver at position 25 (- calcifediol) and in the kidney at position 1 (- calcitriol = vitamin D hormone). 1-Hydroxylation depends on the level of calcium homeostasis and is stimulated by parathormone and a fall in plasma levels of Ca2+ and phosphate. Vitamin D hormone promotes enteral absorption and renal reabsorption of Ca2+ and phosphate. As a result of the increased Ca2+ and phosphate concentration in blood, there is an increased tendency for these ions to be deposited in bone in the form of hydroxyapatite crystals. In vitamin D deficiency, bone mineralization is inadequate (rickets, osteomalacia). Therapeutic use aims at replacement. Mostly, vitamin D is given in liver disease, calcifediol may be indi-... 

Q7 Calcium is present in both intracellular fluid (ICF) and ECF, but the concentration in the ECF is twice as high as that in the ICF. Calcium is found in both ionized and bound forms, and Ca2+ homeostasis is mainly controlled by parathyroid hormone, which increases absorption of calcium in the intestine and reabsorption in the nephron. Calcitonin also affects ECF calcium concentration by promoting renal excretion when there is an excess of calcium in the body. The normal kidney filters and reabsorbs most of the filtered calcium however, in renal disease this is reduced and blood calcium decreases. Calcium and phosphate imbalance can occur in patients with renal failure, leading to osteomalacia (defective mineralization of bone). Osteomalacia is mainly due to reduced production of 1,25-dihydroxycholecalciferol, an active form of vitamin D metabolized in the kidney. Deficiency of 1,25-dihydroxycholecalciferol reduces the absorption of calcium salts by the intestine. 

---