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Serum phosphorus

As renal function declines in patients with CKD, decreased phosphorus excretion disrupts the balance of calcium and phosphorus homeostasis. 0 The parathyroid glands release PTH in response to decreased serum calcium and increased serum phosphorus levels. The actions of PTH include ... [Pg.387]

All of these actions are directed at increasing serum calcium levels and decreasing serum phosphorus levels, although the activity of calcitriol also increases phosphorus absorption in the GI tract and mobilization from the bone, which can worsen hyperphosphatemia. Calcitriol also decreases PTH levels through a negative feedback loop. These measures are sufficient to correct serum calcium levels in the earlier stages of CKD. [Pg.387]

The increased serum phosphorus binds to calcium in the serum, which leads to deposition of hydroxyapatite crystals throughout the body. The calcium-phosphorus (Ca-P) product reflects serum solubility. A Ca-P product greater than 75 mg2/dL2 promotes crystal deposition in the joints and eye, leading to arthritis and conjunctivitis, respectively. Soft tissue deposition primarily affects the coronary arteries of the heart, lungs, and vascular tissue and is associated with a Ca-P product greater than 55 mg2/dL2.36 The Ca-P product has been associated with increased mortality37 and is a risk factor for calcification of vascular and soft tissues.35... [Pg.387]

Increased serum phosphorus levels Low to normal serum calcium levels Increased Ca-P product Increased PTH levels Decreased vitamin D levels... [Pg.388]

Phosphate-Binding Agents When serum phosphorus levels cannot be controlled by restriction of dietary intake, phosphate-binding agents are used to bind dietary phosphate in the GI tract to form an insoluble complex that is excreted in the feces. Phosphorus absorption is decreased, thereby... [Pg.389]

Phosphorus is provided as sodium or potassium phosphate in PN. Approximately 10 to 15 mmol of phosphate are needed per 1000 kilocalories to maintain normal serum phosphorus concentrations (provided the patient is well nourished and has normal renal function).15 Patients with renal insufficiency may require phosphorus restriction. [Pg.1498]

Phosphate-binding agents decrease phosphorus absorption from the gut and are first-line agents for controlling both serum phosphorus and calcium concentrations (Table 76-3). [Pg.881]

Severe hypophosphatemia (serum phosphorus <1 mg/dL) has diverse clinical manifestations that affect many organ systems. [Pg.903]

Asymptomatic patients or those who exhibit mild to moderate hypophosphatemia can be treated with oral phosphorus supplementation with the goal of correcting serum phosphorus concentration in 7 to 10 days (Table 78-4). [Pg.904]

Patients should be closely monitored with frequent serum phosphorus and calcium determinations, especially if phosphorus is given IV or if renal dysfunction is present. [Pg.904]

One explanation for the adverse effects of excessive phosphorus intakes on bone health of rodents is that of secondary hyperthyroidism (4,j>,6). Under these circumstances, PTH activities and cAMP urinary excretions would be expected to increase and blood serum phosphorus would be expected to increase. This in turn would be expected to result in formation of calcium-phosphorus complexes, decrease in serum ionized calcium, parathyroid stimulation and bone resorption. [Pg.91]

Blood serum phosphorus levels were significantly lower when the... [Pg.104]

Serum phosphorus levels responded more dramatically to the meals than did serum calcium. Ingestion of a high protein meal significantly reduced serum phosphorus below those levels obtained when 0 or 15 g of protein was fed. Ingestion of the basal meal elevated serum phosphorus. Therefore, the addition of 45 g of protein to the nutrients in the basal diet negated and reversed the effect on serum phosphorus. Hypophosphatemia has been shown to... [Pg.136]

Renal osteodystrophy is a complex disorder with several pathogenic factors. Histological evidence of bone disease is common in early renal failure and deficits in calcitriol synthesis seems to be an important factor in the pathogenesis of secondary hyperparathyroidism in early CRF. The most common component is osteitis fibrosa manifested as subperiosteal resorption of bone. This is due to decreased excretion as well as increased secretion of parathyroid hormone. In CRF small increments of serum phosphorus cause small decreases in serum calcium. [Pg.612]

Nephrotoxicity characterized by increased serum creatinine and decreased serum phosphorus levels is a treatment-limiting toxicity of adefovir therapy. [Pg.20]

Phosphate-binding compounds maybe needed to control serum phosphorus levels... [Pg.939]

Mechanism of Action An antihyperphosphatemia agent that binds with dietary phosphorus in the GI tract, thus allowing phosphorus to be eliminated through the normal digestive process and decreasing the serum phosphorus level. Therapeutic Effect Decreases incidence of hypercalcemic episodes in patients receiving calcium acetate treatment. [Pg.1123]

Serum phosphorus, calcium, bicarbonate, and chloride levels... [Pg.1124]

Sevelamer For control of serum phosphorus in patients with chronic kidney disease and hemodialysis... [Pg.466]

Conversion of 7-dehydrocholesterol to vitamin D3 and metabolism of D3 to l,25(OH)2D3 and 24,25(OH)2D3. Control of the latter step is exerted primarily at the level of the kidney, where low serum phosphorus, low serum calcium, and high parathyroid hormone favor the production of l,25(OH)2D3, whereas fibroblast growth factor 23 inhibits its production. The inset shows the... [Pg.958]

An epidemiology study (Hughes et al. 1962) compared the mean serum phosphate level of five occupationally-exposed phosphorus plant workers with the mean serum phosphate level of five healthy control men not exposed to phosphorus. The exposure duration ranged from 1 to 17 years in the exposed group. Although the route of exposure was not reported, it is assumed to be inhalation of airborne phosphorus. It is likely that oral exposure (ingestion of airborne phosphorus) also occurred. The serum phosphorus levels of phosphorus plant workers and controls were reported to be 2.85 and 2.9 mg/100 mL, respectively. Both values are below the normal range for adult humans of 3.0 1.5 mg/100 mL (Harper 1969). There was no statistical difference between the workers and controls serum phosphate levels (test and p value not reported). [Pg.107]

The metabolism of phosphorus (P) is largely related to that of calcium (Ca). The Ca P ratio in the diet affects the absorption and excretion of these elements (Harper 1969). Any increase in serum phosphorus results in a decrease of serum calcium by mechanisms which are still unknown. For example, increased serum phosphorus levels and decreased serum calcium levels are seen in uremia (renal retention of phosphorus), hypoparathyroidism, hypocalcemia (decreased serum calcium levels), and hyperphosphatemia (increased serum phosphorus levels), and the reverse is seen in hypercalcemia (increased serum calcium levels) and hyperparathyroidism. Hypophosphatemia (low serum phosphorus levels) is seen in ricketts (vitamin D deficiency) (Harper 1969 Tietz 1970). [Pg.115]

The recommended ratio of phosphorus to calcium is 1 1, except in infants it is 2 1. For older infants, the recommended intake of phosphorus is increased to 80% of the calcium requirement, so that the ratio is similar to cow s milk (Harper 1969). Both phosphorus and calcium are distributed similarly in foods, hence a sufficient intake of calcium ensures a sufficient intake of phosphorus. The exception is cows milk, which contains more phosphorus than calcium (Harper 1969). The adult daily requirement for phosphorus is about 700 mg. A balanced diet provides sufficient amounts of phosphorus because it is commonly found in foods (phosphoproteins and phospholipids, inorganic phosphate), especially milk and milk products, wheat, meats and fish (Latner 1975). In the body, normal serum (inorganic) phosphorus levels are 4-7 mg/100 mL in children and 3-4.5 mg/100 mL in adults and the elderly. In body fluids and tissues, normal serum phosphorus levels found are 40, 170-250, 360, and 22,600 mg/100 mL in blood, muscle, nerve, and both bones and teeth, respectively (Harper 1969 Tietz 1970). [Pg.115]


See other pages where Serum phosphorus is mentioned: [Pg.606]    [Pg.388]    [Pg.389]    [Pg.391]    [Pg.414]    [Pg.415]    [Pg.415]    [Pg.1504]    [Pg.96]    [Pg.104]    [Pg.126]    [Pg.134]    [Pg.135]    [Pg.137]    [Pg.137]    [Pg.1706]    [Pg.1795]    [Pg.282]    [Pg.243]    [Pg.613]    [Pg.282]    [Pg.194]    [Pg.509]    [Pg.310]   
See also in sourсe #XX -- [ Pg.173 ]




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