Urinary calcium excretion dietary

For more than forty years, it has been known that increasing the protein content of the diet causes an increase in urinary calcium excretion (1, 2). There is, in fact, a direct correlation between urine calcium output and dietary protein level, so that excretion is 800 percent higher if dietary protein is increased from 6 g per day to 560 g per day (3 ). This relationship between urinary calcium and protein ingestion is not affected by the level of dietary calcium, and is evident even when severely calcium-deficient diets are consumed (3). 

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. 

Increasing the dietary calcium level in the high beef meal resulted in hypercalciuria. This effect was obtained in the absence of an altered insulin response which suggests that factors other than or in addition to serum insulin were involved in the control of urinary calcium excretion. 

As intestinal absorption of calcium increases, urinary calcium excretion also increases. When the latter exceeds 300 mg/d, formation of calcium phosphate or calcium oxalate stones (urolithiasis) may occur. Hypercalciuria may result from decreased reabsorption of calcium due to a renal tubular defect or from increased intestinal absorption of calcium. Hypercalciuria may be due to an intrinsic defect in the intestinal mucosa or secondary to increased synthesis of 1,25-(OH)2D in the kidney. Disordered regulation of 1,25-(0H)2D synthesis is relatively common in idiopathic hypercalciuria. Treatment usually includes reduction in dietary calcium. Increased vitamin D intake, hyperparathyroidism, and other disorders can also cause hypercalciuria and urolithiasis. 

Garland, H.O., A.G. Porshaw, and C.P. Sibley. 1997. Dietary essential fatty acid supplementation, urinary calcium excretion and reproductive performance in the diabetic pregnant rat. J. Endocrinol. 153(3) 357-363. 

A single dose of 500 ml cranberry juice had no effect on urinary oxalate secretion but significantly increased mean urinary calcium levels (Brinkley et al. 1981). A significant increase in urinary calcium excretion was observed in a small study after consumption of 2 pints of cranberry juice (Kahn et al. 1967). Consumption of 2 pints daily of cranberry juice for 1 month reduced urinary ionized calcium by 50% (Light et al. 1973). A study on dietary intake and urinary excretion of oxalates indicated that cranberry juice had no effect on oxalate excretion (Massey et al. 1993). 

Collectively, the possible effects of high dietary intakes of protein and phosphate on urinary calcium excretion and enhanced bone resorption, respectively, along with the possibility of reduced calcium absorption with advancing age, argue for recommending an ample intake of calcium. 

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. 

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. 

Earlier animal work showed similar results in terms of urinary acid production from dietary precursors that could be converted into acid before excretion. However, most investigators used salts rather than foods containing the anion or its precursor. The addition of acid, in the form of hydrochloric, sulfuric, or ammonium chloride, acid phosphate salts, or ascorbate resulted in enhanced urinary acidity and concomitant calcium excretion. For example, in the detailed study of bone salt metabolism, Barzel and Jowsey (19) showed that the rat fed supplementary ammonium chloride subsequently lost more calcium, and developed markedly demineralized fat-free bone mass. 

Acidosis resulting from endogenous acid production also induces urinary calcium loss. The kidney responds to such acid production, as in the case of dietary acid, by excreting more calcium. 

Since this increased calcium loss, the quality of dietary protein may be important in conserving body calcium in the bone reservoir via the kidney. Human renal studies have corroborated animal data in-so-far as calcium excretion as influenced by urinary acidity is concerned. This was emphasized by Marone et al. (15) who reported increased excretion of calcium in the acidotic dog and by Zemel, et al. (27) who studied calcium filtration by the kidney. They fed subjects low or high-protein (50 or 150 g/d) diets, then compared... 

Liebman, M., and Chai, W. (1997). Effect of dietary calcium on urinary oxalate excretion after oxalate loads. Am. ]. Clin. Nutr. 65,1453-1459. 

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). 

With the typical dietary intake of calcium (800 mg/day), about 20% of the calcium is absorbed. Fecal Ca is about 640 mg/day and urinary Ca is about 160 mg/day. Urinary calcium increases somewhat with an increase in intake. For any given increase, urinary Ca increases by an amount equivalent to about 6,0% of the increase in intake. Fecal Ca consists of the unabsorbed mineral and a small amount of Ca secreted into the gastrointestinal tract (100-150 mg/day). An amount of Ca equivalent to 1 to 6% of the total fecal Ca is excreted in the bile I eGrazia and Rich, 1964). Urinary Ca generally ranges from 100 to 250 mg/day. The Ca lost via the skin is about 15 mg/day, with increased losses occurring in the sweat during work in warm climates. 

The mechanism by which dietary protein induces an increase in urinary calcium is not clear. The effect has been attributed, in part, to the catabolism of sulfur-containing amino acids to yield sulfate. Elevated levels of plasma sulfate can form a complex with calcium. The complex passes into the renal tubule, where it is poorly reabsorbed, resulting in its excretion in the urine. The mechanism by which phosphate reverses the h5rpercalciuric effect of protein is also not clear. 

Other methods used to decrease the recurrence of urolithiasis include dietary modifications that decrease calcium excretion and promote diuresis. Changing the diet from alfalfa to grass or oat hay decreases the calcium intake and should decrease the urinary excretion of calcium, since fecal calcium excretion is relatively constant in horses. Although this dietary change should decrease the total calcium excretion, it may also decrease the urinary excretion of nitrogen and the daily urine volume. The latter changes could enhance the supersaturation of urine. In theory, diuresis could be promoted further by the addition of loose salt (50-75 g per day) to the concentrate portion of the diet. However, in one study where ponies were fed sodium chloride (1, 3 or 5% of the total diet dry matter (1% is approximately 75 g sodium chloride for a 500 kg horse)), there were no differences in water intake, urine production or calcium excretion. 

There is only one study of the dietary intake and excretion of uranium at naturally occurring concentrations under strictly controlled conditions [24], In that study four nonoccupationally exposed persons received a diet containing 1.6 p,g U/day (20 mBq/day). The water intake of each person varied, ranging from 0.5 to 2.1 p-g/day (6-26 mBq/day). All excreta were collected and pooled samples from each person were analyzed for uranium and stable calcium. The metabolic balances showed that the majority of the uranium was passed via the intestine, most probably unabsorbed. Some excretion occurs from blood into the intestine, via bile, the so-called endogenous excretion. Urinary uranium excretion ranged from 0.01 to 0.1 (xg/day (0.15-1.0 mBq/day) and was linearly correlated with the quantity of uranium consumed from water. The urinary excretion equation was... 

Excess dietary protein also leads to an increase in urinary calcium in adult rodents, but there is no attendant loss of calcium from the skeleton or negative calcium balance. This difference between species appears to be due to two factors a smaller fractional excretion of endogenous calcium in the urine of rodents (less than 5%) and a greater capacity to buffer metabolic acid. Only when acid loads are sufficient to depress... 

Since excess dietary protein and excess phosphorus have opposing effects on urinary calcium, the natural association of these nutrients in the human diet tends to ameliorate the effect of both on calcium excretion and bone loss. Whether the relative amounts of protein and phosphorus in high protein diets are always compatible with calcium homeostasis is unclear. This question is not amenable to study in rodents because feeding excess protein has no effect on calcium balance. Excess phosphorus causes bone loss irrespective of the protein content of the diet. Hence, adult rodents and adult humans differ with respect to their skeletal response to both excess protein and excess phosphorus. 

The amount of calcium excreted in the urine is related to skeletal size, the acid-base regulation of the body, and the dietary protein intake. Urinary excretion of calcium rises when dietary protein is increased and falls when dietary protein is decreased, it appears that calcium losses can be substantial when protein intake is high hence, if this type of diet is continued for a prolonged period, it could result in a considerable loss of body calcium and even osteoporosis. FHow-ever, studies show that a high protein intake from a high meat diet has little effect on calcium excretion, possibly because of the high phosphate intake with the meat diet. A recent study suggests that increased phosphorus intakes reduce urinary excretion of calcium and lower serum calcium levels. 

Massey, L. K., Wise, K. J., The effect of dietary caffeine on urinary excretion of calcium, magnesium, sodium and potassium in healthy young females, Nutrition Research, 4, 43, 1984. 

Morgan et al. (M3) examined the effect of the administration of EDTA in idiopathic hypercalcemia. Given orally, a dosage of up to 3 g daily resulted in a fall in the serum calcium level. Given subcutaneously in a dosage of 1 g daily, there was a fall in calcium retention in a balance study, a retention of 51 % being converted to a retention of 28 % on similar dietary intakes of calcium. There was an increase in the urinary excretion of calcium. 

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