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Phosphorus excretion levels

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]

As kidney function continues to decline and the GFR falls less than 60 mL/minute/1.73 m2, phosphorus excretion continues to decrease and calcitriol production decreases, causing PTH levels to begin to rise significantly, leading to secondary hyperparathyroidism (sHPT). The excessive production of PTH leads to hyperplasia of the parathyroid glands, which decreases the sensitivity of the parathyroid glands to serum calcium levels and calcitriol feedback, further promoting sHPT. [Pg.387]

Significantly more phosphorus was excreted in the feces when 1.2% calcium and 1.2% phosphorus diets were fed with either egg white (317 mg) or soy (303 mg), than when any of the other rations were fed. Orthogonal contrast analysis indicated that statistically significant sources of these differences included ration phosphorus level (P <0.001), calcium level (P< 0.0001), and calcium level x protein source (P< 0.0461). The degree of effectiveness of increasing phosphorus excretion with increased ration level of calcium was greater in egg white fed animals than in soy fed animals. [Pg.97]

Figure 7. The effect of different ration levels of calcium (Ca = O.37o and Ca = 1.27o) and phosphorus (Pi = 0.37> and P2 = 1.27 ) on urinary phosphorus- excretion of mice fed soy (S) or egg white (E) protein. P-protein interaction P < 0.0039. Figure 7. The effect of different ration levels of calcium (Ca = O.37o and Ca = 1.27o) and phosphorus (Pi = 0.37> and P2 = 1.27 ) on urinary phosphorus- excretion of mice fed soy (S) or egg white (E) protein. P-protein interaction P < 0.0039.
High levels of dietary zinc were associated with marked decreases in bone calcium deposition and in the apparent retention of calcium in male weanling albino rats. Marked increases in fecal calcium levels were also observed in the zinc-fed rats. Excessive dietary zinc was associated with a shifting of phosphorus excretion from the urine to the feces. This resulted in an increase in fecal phosphorus and provided an environmental condition which would increase the possibility of the formation of insoluble calcium phosphate salts and a subsequent decrease in calcium bioavailability. The adverse effect of high dietary zinc on calcium status in young rats could be alleviated and/or reversed with calcium supplements. [Pg.165]

The data presented in this paper indicate that excess levels (0.75%) of dietary zinc result in decreases in the bioavailability of calcium and phosphorus in rats and interfere with normal bone mineralization. High dietary levels of calcium or zinc appeared to cause a shift in the excretion of phosphorus from the urine to the feces, while the presence of extra phosphorus tended to keep the pathway of phosphorus excretion via the urine. The presence of large amounts of phosphorus in the Intestinal tract due to high intakes of zinc would increase the possibility of the formation of insoluble phosphate salts with various cations, including calcium, which may be present. A shift in phosphorus excretion from the feces to the urine, however, could result in an environmental condition within the system which would tend to increase the bioavailability of cations to the animal. The adverse effect of zinc toxicity on calcium and phosphorus status of young rats could be alleviated with calcium and/or phosphorus supplements. [Pg.172]

Mechanism of Action A bisphosphonate that inhibits the resorption of mineralized bone and cartilage inhibits increased osteoclastic activity and skeletal calcium release induced by stimulatory factors produced by tumors. Therapeutic Effect Increases urinary calcium and phosphorus excretion decreases serum calcium and phosphorus levels. [Pg.1323]

The amount of phosphorus excreted in the urine vanes with the level of ingested phosphorus and factors influencing phosphorus availability and utilization. It has been shown that in the dog, when plasma phosphate is normal or low, over 99% of the filtered ion is reabsorbed, presumably in die upper part of the proximal tubule. Increased plasma concentrations of alanine, glycine, and glucose depress phosphate reabsorption. [Pg.1283]

The amount that fecal phosphorus levels decline with phytase supplementation will depend on the percentage of phosphorus that is available in the base ration (Yi, 1996b). With available phosphorus at 0.05% of the ration in this study, excretion of phosphorus was reduced by about 25% in pigs receiving phytase compared to the control animals. When the base diet in this study contained 0.16% available phosphorus, excretion was reduced by 50% in pigs receiving phytase but no inorganic phosphorus. [Pg.155]

Phosphorus is more readily absorbed from the intestinal tract than calcium. Approximately two-thirds of the phosphorus excreted is found in the feces, one-third in the urine. Between 10 and 20 % of phosphorus is found in tissues other than bone, and this phosphorus appears to have metabolic priority. The mechanisms which regulate deposition and release of phosphorus from bone are the same as those for calcium. Phosphorus in soft tissues plays a very vital role in many metabolic processes. The importance of adenosine triphosphate (ATP) in energy transfer systems has been discussed previously (p. 203, Chapter 16). Phosphorylation appears to be essential for the absorption of a number of nutrients, e.g., fatty acids and glucose. The phosphate radical is bound to proteins, fatty acids, carbohydrates, and enzymes. Phosphate is the chief inorganic anion of intracellular fluid, and phosphates of extracellular fluid participate in acid-base regulation. The inorganic phosphate level of blood ranges from 2 to 4 mg. per 100 ml. in adults and 3 to 5 mg. per 100 ml. in children. [Pg.539]

Blood urea nitrogen (BUM) levels are elevated and the urine specific gravity is low. Urinary phosphorus excretion is reduced and hyperkalemia is seen. [Pg.318]

Schoeninger, M.J. and DeNiro, M.J. 1984 Nitrogen and carbon isotopic composition of bone collagen from marine and terrestrial animals. Geochimica et Cosmochimica Acta 48 625-639. Schuette, S. A., Hegsted, M., Zemel, B. and Linkswiler, H.M. 1981 Renal acid, urinary cyclic AMP, and hydroxyproline excretion as affected by level of protein, sulfur amino acids and phosphorus intake. Journal of Nutrition 111 2106-2116. [Pg.258]

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]

The rat has been used rather widely to study the relation between dietary protein, or acid salt feeding, and calcium loss. Barzel and Jowsey (19) showed that the rat fed a control diet supplemented with ammonium chloride excreted excessive urinary calcium, and experienced a concomitant loss of fat-free bone tissue. Draper, et al. (20) extending this work, reported an inverse relation between dietary phosphate and loss of bone calcium and dry, fat-free tissue. In subsequent studies (21), they reported that this process was accompanied by reduced serum calcium levels the high phosphorus, low calcium diet increased urinary calcium loss. Whereas, increasing the phosphorus content of the diet stopped the excessive urinary calcium loss. To test possible zinc loss that might result from this sort of acid salt feeding, Jacob and her coworkers (22) fed rats a supplement of ammonium chloride and then measured urinary zinc and calcium. The hypercalciuria occurred exclusive of an effect upon urinary zinc loss. [Pg.77]

The results of experiments conducted by MacKenzie and McCollum (15) indicate that the effect of dietary oxalic acid on the rat depends on the composition of the diet. There was no effect on rate of growth or calcium excretion of 50 g rats fed for 10 weeks a diet containing 0.6% calcium, 0.7% phosphorus, and optimum vitamin D, when levels of potassium oxalate up to 2.5% were fed. The percent bone ash on the 2.5% oxalate diet was somewhat lower than on the control diet. On a 0.35% calcium, 0.35% phosphorus, and vitamin D-free diet, 1.7% potassium oxalate resulted in restricted growth and bone formation of weanling rats. [Pg.107]

The effects of varying either the calcium or phosphorus level in conjunction with a high beef meal on the urinary calcium excretion of men are shown in Table IV. Urinary calcium excretion (total and ionized) was significantly elevated (P < 0.005) when the high protein beef meal contained 466 mg rather than 166 mg calcium. Increasing the phosphorus level from 308 mg to 700 mg in the high beef meal reduced both total and ionized calcium excretion in the urine, but the response was not statistically significant. Serum levels of calcium (ionized and total) and phosphorus were within normal limits and were unaffected by any of the dietary treatments. [Pg.130]

Table VII shows the calcium balance of zinc-fed and non-zinc-fed rats supplemented with 0.8% calcium and/or phosphorus. Marked increases in fecal calcium and corresponding decreases in apparent calcium retentions in the zinc-fed rats could be reversed with calcium supplementation. Phosphorus supplements appeared to be associated with increases in calcium retention in the absence of zinc, but decreases in calcium retention in the presence of zinc without calcium supplementation. Decreases in fecal calcium were noted in animals fed calcium supplements in the presence of phosphorus or zinc. High levels of zinc were associated with increases in fecal calcium excretion in the absence of extra calcium or in the presence of extra phosphorus. Calcium supplementation was generally associated with a decrease in the urinary excretion of calcium, while zinc and phosphorus supplements were generally associated with an increase in urinary calcium excretion. Table VII shows the calcium balance of zinc-fed and non-zinc-fed rats supplemented with 0.8% calcium and/or phosphorus. Marked increases in fecal calcium and corresponding decreases in apparent calcium retentions in the zinc-fed rats could be reversed with calcium supplementation. Phosphorus supplements appeared to be associated with increases in calcium retention in the absence of zinc, but decreases in calcium retention in the presence of zinc without calcium supplementation. Decreases in fecal calcium were noted in animals fed calcium supplements in the presence of phosphorus or zinc. High levels of zinc were associated with increases in fecal calcium excretion in the absence of extra calcium or in the presence of extra phosphorus. Calcium supplementation was generally associated with a decrease in the urinary excretion of calcium, while zinc and phosphorus supplements were generally associated with an increase in urinary calcium excretion.
A high proportion of the phosphorus present in feedstuff s may be in the form of phytate, which is poorly digested by birds because they lack the requisite enzyme in the gut. Consequently, the content of non-phytate phosphorus in feed ingredients is used in formulating poultry diets to ensure the required level of phosphorus, rather than the total phosphorus content. It is now becoming a common practice for a microbial phytase to be added to conventional poultry diets. This achieves a greater release of the bound phosphorus in the gut and a reduced amount to be excreted in the manure and into the environment. Use of microbial phytase may also improve digestion of other nutrients in the diet, associated with breakdown of the phytate complex. [Pg.30]

The serum phosphate level of a worker with phossy jaw was within the normal range of values for an adult human (Hughes et al. 1962). Excretion of phosphate via urinary and fecal routes was reported qualitatively to be approximately normal. The daily output of phosphorus in the feces was about 1/4 to 1/3 of the total output in both urine and feces. [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]

White Phosphorus. The pharmacokinetics database is inadequate. No quantitative information was located regarding absorption, distribution, metabolism, or excretion following inhalation, dermal, and dermal burn exposure to white phosphorus. Definitive quantitative data on metabolic pathways following oral exposure to white phosphorus also are lacking. Data that were located on absorption, distribution, and excretion following oral exposure were helpful. They provided some time-related data, but provided no information regarding comparisons between various dose levels. [Pg.167]

Limited data are available about the effects of individual dietary components on absorption, and consequently the requirement, of Mn. Dietary protein and phosphorus levels (33), calcium level (34) and the effect of a partial substitution of soy protein for meat (28) have been tested in balance studies without any obvious effect of Mn absorption or retention. However, since the main route of excretion is via the bile, the conventional balance technique is probably not sensitive enough to identify dietary factors that influence Mn absorption. [Pg.15]


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