Phosphorus excretion

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 ... 

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. 

The most common cause of hyperphosphatemia is decreased phosphorus excretion, secondary to decreased glomerular filtration rate. 

Table VIII. Phosphorus Excretion and Retention as Affected by Orthophosphate, Hexametaphosphate (Polyphosphate), and Calcium...

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. 

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. 

Table VI shows the effect of 0.75% dietary zinc on the phosphorus balance in young rats. A decrease in the apparent retention of phosphorus was noted in the zinc-fed rats as early as the end of the first week. Possibly a more significant observation was the apparent movement of phosphorus excretion from the urine, the normal pathway for phosphorus excretion, to the feces in rats fed the high zinc diet. Such a shifting of the phosphorus excretion to the fecal pathway in animals fed a high zinc diet should result in an increase...

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. 

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. 

In comparison, our measurements of epilimnetic zooplankton biomass over the study period (3540 mg/m2), combined with Scavia s (7) weight-specific zooplankton regeneration rate of 1.7 xg of P/mg per day, give a flux of —800 mg of P/m2. These estimates of phosphorus excretion rates are similar to our carbon-based phosphorus demand. 

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. 

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. 

T. C. Schell, Phytase supplementation of low-phosphorus growing-finishing pig diets improves performance, phosphorus digestibility, and bone mineralization and reduces phosphorus excretion, J. Anim. Sci. 1997, 75, 3174-3186. 

Some mechanisms contributing to bone mineral homeostasis. Calcium and phosphorus concentrations in the serum are controlled principally by two hormones, l,25(OH)2D3(D) and parathyroid hormone (PTH), through their action on absorption from the gut and from bone and on excretion in the urine. Both hormones increase input of calcium and phosphorus from bone into the serum vitamin D also increases absorption from the gut. Vitamin D decreases urinary excretion of both calcium and phosphorus, while PTH reduces calcium but increases phosphorus excretion. Calcitonin (CT) is a less critical hormone for calcium homeostasis, but in pharmacologic concentrations CT can reduce serum calcium and phosphorus by inhibiting bone resorption and stimulating their renal excretion. Feedback effects are not shown. 

Ryabushko, V.I. and Propp, L.N. (1985). Respiration and nitrogen and phosphorus excretion by echinoderms from the South China Sea (In Russian). Biologiya Morya (6), 42-46. 

White Phosphorus. No studies were located that specifically address white phosphorus excretion in humans after oral exposure However, two animal studies (Cameron and Patrick 1966 Lee et al. 1975) indicate rapid urinary and fecal excretion of white phosphorus, metabolites, or unabsorbed inorganic breakdown products. 

The phosphorus balance data (Table II) show that the urinary phosphorus excretion Increased approximately two- to three-fold In all three high phosphorus studies, while the fecal phosphorus excretion Increased to a considerably lesser extent. The phosphorus balance of all three patients became more positive during the high phosphorus Intake. These studies have shown that Increasing the phosphorus Intake up to 2000 mg/day did not affect the excretions of zinc nor the zinc balance, despite the fact that there were marked changes In phosphorus metabolism, primarily a marked Increase of the urinary phosphorus excretion, while the fecal phosphorus excretion Increased to a lesser extent. 

Szyper, J. P. (1981). Short-term starvation effects on nitrogen and phosphorus excretion by the chaetognath Sa ita eijlata. Estuar. Coast. Shelf Sci. 13, 691—700. 

Lean D. R. S. and Nawelajko C. (1976) Phosphate exchange and organic phosphorus excretion by freshwater algae. J. Fish. Board. Can. 33, 1312. 

Hyperphosphatemia occurs without specific clinical signs in horses with strangulating intestinal lesions (Arden Stick 1988) and severe colitis (Svendsen et al 1979). The clinical findings reported in small animals include diarrhea, hypocalcemia, hypernatremia and an increased propensity to metastatic soft-tissue calcification. The treatment recommended in small animals includes i.v. fluids to correct any acidosis and promote renal phosphorus excretion and dextrose-containing fluids to promote translocation of phosphorus into cells (Macintire 1997). 

Serum phosphorus concentration is so closely regulated by the kidneys that it is unusual for hyperphosphatemia (serum phosphorus concentration >4.5 mg/dL) to develop in patients with normal renal function. The most frequent causes of hyperphosphatemia are decreases in urinary phosphorus excretion, and increases in phosphate entrance into the extracellular fluid via either exogenous administration or endogenous intracellular phosphate release. 

The most common cause of hyperphosphatemia is a decrease in urinary phosphorus excretion secondary to decreased glomerular filtration rate. ° Retention of phosphorus decreases vitamin D synthesis and induces hypocalcemia, which leads to an increase in PTH. This physiologic response inhibits further tubular reabsorption of phosphorus to correct hyperphosphatemia and normalize serum calcium concentrations. Patients with excessive exogenous phosphorus administration or endogenous intracellular phosphorus release in the setting of acute renal failure may develop profound hyperphosphatemia. Severe hyperphosphatemia is commonly encountered in patients with chronic kidney disease, especially those with GFRs less than 15 mL/ min per 1.73 m (see Chap. 44). 

Hypoparathyroidism results in increased renal tubular reabsorption of phosphorus and may result in hyperphosphatemia. Hyperphosphatemia associated with hypoparathyroidism is usually less severe than that associated with severe renal failure or excessive exogenous or endogenous introduction of phosphorus into the ECR Hypoparathyroidism is the most important cause of increased tubular phosphorus reabsorption. Acromegaly and thyrotoxicosis may also cause hyperphosphatemia by reducing urinary phosphorus excretion. 

Any disorder that results in necrosis of skeletal muscle cells (i.e., rhabdomyolysis) can result in the release of large amounts of intracellular phosphorus into the systemic circulation. This condition is frequently associated with acute renal failure and thus severe hyperphosphatemia may develop due to increased endogenous phosphorus release coupled with decreased renal phosphorus excretion. Bowel infarction, malignant hyperthermia, and severe hemolysis are also conditions that may increase endogenous release of phosphorus. 

Parathyroidectomy is followed by a fall in urine phosphate excretion and a consequential rise in plasma inorganic phosphate concentration until a new equilibrium is established (Tl). In clinical hypoparathyroidism, plasma inorganic phosphate may be as high as 10 mg/100 ml, but the amount of phosphorus excreted in the urine by such patients really depends upon dietary intake. In these cases, therefore, phosphate clearance is usually low and is always low when considered in relation to the plasma phosphate concentration (K4, N6, Nil). 

A wide range of plasma phosphorus concentration has been observed by other workers in primary hyperparathyroidism (C7) and explained in terms of diet and renal excretion. Unlike the calcium concentration, which is normally very constant regardless of dietary intake and urinary excretion, the concentration of inorganic phosphate in plasma is the resultant of the rate of phosphorus absorption from the gut and protein catabolism, on the one hand, and of renal excretion, on the other. Although the parathyroid hormone promotes phosphorus excretion, this is only one of the factors governing plasma phosphate concentration. Plasma phosphate in cases of hyperparathyroidism on a relatively high phosphorus intake may therefore not be distinguishable from that in normal subjects on a lower intake. 

Suppression of phosphorus excretion by infusion of calcium can also be used as a diagnostic test. It was first introduced for this purpose by... 

Diez, L, C. C. Perez, M. B. Garcia, M. J. Cano, and M. A. Rios. 1996. Twenty-four-hour urinary calcium and phosphorus excretion in beagle dogs. Preliminary report. Scandinavian Journal of Laboratory Animal Science 23 355-362. 

Phytase is in this category of enzyme. It releases the orthophosphate groups from phytic acid, which is only partially broken down by non-ruminants and is the major form of phosphorus in cereal grains and oilseeds (see p. 115).This results in a greater availability of phosphorus to the animal, and the amount of inorganic phosphorus added to the diet can be reduced, with beneficial effects on the environment through reduced phosphorus excretion. 

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