Urinary phosphorus excretion

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.

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. 

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. 

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

The meat diet resulted in markedly greater titratable acid and calcium excretion compared with the soy diet (P<0.02). This occurred despite the fact that each diet contained the same amounts of protein, calcium, phosphorus, and sulfur. Increased urinary calcium excretion in subjects accompanied this increased output of TTA (P<0.02) ... 

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. 

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.

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. 

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. 

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. 

Table II shows data of the effect of a high phosphorus Intake on the zinc balance. The phosphorus supplements were given to three patients during different calcium Intakes, namely, during a low calcium Intake of 200 mg per day and during higher calcium Intakes of 800 mg and 2000 mg calcium per day. The phosphorus Intake of the subjects studied was approximately 900 mg per day In the control study and was 2000 mg per day during the high phosphorus Intake. In the control study, during a low calcium Intake and a normal phosphorus Intake of 900 mg per day and a dietary zinc Intake of 17 mg per day, the urinary zinc excretion was relatively high, 1.6 mg/day, the fecal zinc excretion was In the expected range and the zinc balance was positive,...

Studies of the effect of both calcium and phosphorus on the zinc balance which have been carried out In this Research Unit (19. 20) have shown that the zinc balance varies during a normal dietary calcium and phosphorus Intake and ranges from slightly negative to positive values and that the net or apparent absorption of zinc, calculated from zinc balance data, remained unchanged during the addition of the amounts of calcium or phosphorus used In these studies. The zinc balances In the present study have to be considered as maximal balances as the loss of zinc In sweat has not been considered as part of the excretory losses. It has been estimated that the loss of zinc In sweat Is quantitatively as great as the urinary zinc excretion (21). 

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. 

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. 

Most of the calcium that is lost from the body is excreted in the faeces, this being mainly unabsorbed dietary calcium. However, the digestive secretions all contain small amounts of calcium, and individuals on a calcium-free diet continue to excrete faecal calcium. The normal daily excretion is of the order of 0-1-0-3 g (2-5-7-5 mmol). The quantity of phosphorus excreted daily varies with the dietary intake. As with calcium an appreciable proportion of ingested phosphorus remains unabsorbed and is eliminated in the faeces. Phosphorus is also excreted in the urine, almost entirely in the form of orthophosphates (e.g. NaH2P04 and Na2HP04). Their role in the regulation of acid-base balance is discussed on page 395. Urinary excretion of phosphate is increased in hyperparathyroidism. 

This hormone is secreted by the parathyroid glands, which are four in number and lie on the posterior surface of the thyroid gland. The exact manner in which the hormone exerts its action upon calcium and phosphorus metabolism has not been proved satisfactorily, but the most immediate effect of administration of parathyroid extract which has been generally observed is an increased excretion of phosphorus in the urine, which is accompanied by a lowering of the serum inorganic phosphate. The increase in the urinary phosphate excretion has been ascribed by Harrison and Har-... 

It has been generally established that thyroid dysfunction leads to a disturbance of mineral metabolism. In hyperthyroidism an increased excretion of calcium and phosphorus is constantly found which is diminished by iodine medication and is still further diminished after subtotal thyroidectomy. The high urinary calcium excretion also returns to normal after about 14 days treatment with the antithyroid drug thiouracil. A high fecal excretion of calcium has also been reported but is not a clearly established feature of hyperthyroidism. Long-standing untreated hyperthyroidism is accompanied by an osteoporosis, the cause of which is still a matter of differing opinion. 

Dietary calcium has a relatively small impact on urinary calcium (e.g., only 6-8% of an increase in dietary calcium intake will appear in the urine). The major food components that affect urinary calcium are protein, phosphorus, caffeine, and sodium. For each 50-g increment in dietary protein, approximately 1.5 mmol (60 mg) of additional calcium is lost in urine. The higher amounts of phosphorus consumed concurrently with a high-protein diet can blunt, but not eliminate, this phenomenon. Dietary phosphorus (as well as intravenously administered phosphorus) increases PTH synthesis and subsequently stimulates renal calcium reabsorption and reduces the urinary excretion of calcium. Caffeine causes a reduction in renal reabsorption of calcium and a subsequently increased loss of urinary calcium soon after it is consumed. It has been shown repeatedly in animals and humans that dietary sodium, in the form of salt (NaCl), increases urinary calcium excretion. On average, for every 100 mmol (2300 mg) of sodium excreted in urine, there is an approximately 0.6-1 mmol (24-40 mg) loss of calcium in free-living healthy populations of various ages. Because most of the urinary calcium is of bone origin, it is commonly hypothesized that those nutrients or food components that are hypercalciuretic are also detrimental to the skeleton. On the other hand, thiazide medications are hypocalciuric and, as such, may have modest positive effects on bone. 

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. 

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. 

Diet Phosphorus Intake Fecal Excretion Urinary Excretion Balance... 

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. 

---