Calcium excretion supplements

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.

The suppression of PTH secretion from the parathyroid gland that accompanies the constitutive activation of the CASR makes the disorder difficult to recognize and treat. In some cases, it has been reported that seizures can be intractable. The abnormal set point of calcium regulation complicates treatment with calcitriol and dietary calcium supplementation because the CASR expressed in the kidney controls calcium excretion. The constitutively activated CASR mutant induces hypercalciuria, which may compound the hypocalcemia (42). 

Prentice, A., Jaqou, L. M., Cole, T. J., Stirling, D. M., Dibba, B., and Fairweather-Tait, S. (1995). Calcium requirements of lactating Gambian mothers Effects of a calcium supplement on breast-milk calcium concentration, maternal bone mineral content, and urinary calcium excretion. Am. J. Clin. Nutr. 62, 58-67. 

Comparative effects of calcium lactate and milk on apparent manganese utilization by humans are shown on Table II (7). In this study, 10 adult human subjects were fed 900 mg calcium from milk or 916 mg of calcium from calcium lactate/subject/day. Calcium provided by the basal diet was maintained constant. The increase in fecal manganese excretion with the calcium lactate supplemented diet in comparison to values when milk was the supplemental manganese source suggests that calcium supplied by milk had a lesser adverse effect on manganese absorption than did that from calcium lactate (Table II). 

Adverse effects of oral calcium and vitamin D supplementation include hypercalcemia and hypercalciuria, especially in the hy-poparathyroid patient, in whom the renal calcium-sparing effect of parathyroid hormone is absent. Hypercalciuria may increase the risk of calcium stone formation and nephrolithiasis in susceptible patients. One maneuver to help prevent calcium stones is to maintain the calcinm at a low normal concentration. Monitoring 24-hour urine collections for total calcium concentrations (goal <300 mg/24 h) may also minimize the occurrence of hypercalciuria. The addition of thiazide dinretics for patients at risk for stone formation may result in a reduc-tionof both urinary calcium excretion and vitamin D requirements." ... 

After initial potassium deficits are replaced, ongoing potassium supplementation may not be required, as renal potassium losses decrease following initiation of appropriate alkali therapy. The use of potassium alkali salts may, however, be desirable in patients with associated nephrolithiasis, because sodium salts may increase urinary calcium excretion. 

Since unresolved nephrocaldnosis may lead to residual abnormalities in the kidney induding microscopic hematuria, hypercalciuria, and impaired tubular function [109, 113, 114], renal ultrasonography within a few months of initiating loop diuretics may be warranted [109,113]. If long-term diuretic therapy is needed, a thiazide diuretic alone or in combination with furosemide may reduce the risk of renal calcifications by decreasing urinary calcium and oxalate excretion [109, 111, 113,117,118]. However, two studies of premature infants failed to show a reduction in either urinary oxalate or calcium excretion when thiazides were added to furosemide therapy [116,119]. The lack of beneficial response may have been due to replacement of the infants sodium losses with large amounts of supplemental sodium. 

Knapen, M.H., Hamulyak, K., and Vermeer, C. (1989). The effect of vitamin K supplementation on circulating osteocalcin (bone Gla protein) and urinary calcium excretion, Ann. Intern. Med., Ill, 1001. 

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. 

Epidemiologic studies have consistently documented that increased potassium intake is associated with greater bone mineral density. In trials, supplemental potassium bicarbonate reduced bone turnover as manifest by less urinary calcium excretion and by biochemical evidence of greater bone formation and reduced bone resorption. However, no trial has tested the effect of increased potassium or diets rich in potassium on bone mineral density or clinical outcomes related to osteoporosis. 

Oral bisphosphonates are poorly absorbed (less than 5%). Taking them in the presence of food or calcium supplementation further reduces absorption. After absorption, bisphosphonate uptake to the primary site of action is rapid and sustained. Once attached to bone tissue, bisphosphonates are released very slowly. These drugs are not metabolized and are excreted renally. They are not recommended for use in patients with renal insufficiency. 

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. 

In studies on test meals, Walker et al. (32) discovered that the calcium of Swiss chard, which has a high oxalic acid content, was poorly absorbed. Children excreted more calcium during the 6 hours after a test meal of milk, Pumpkin leaves, cassava leaves, or pigweed leaves than after Swiss chard. All supplements contained 200 mg calcium. 

Based on limited epidemiologic evidence, fluoride supplements, with or without calcium, estrogen and vitamin D, are used by clinicians for the treatment of osteoporosis. However, knowledge of the effects of fluoride on calcium and phosphorus metabolism in normal animals is limited although Spencer et al. (32) reported that ingestion of fluoride by three osteoporotic men did not affect calcium absorption but caused a decrease in urinary excretion. Moreover, there is a need to determine the long-term effects of fluoride treatment on bone strength and on soft tissues ( ). 

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. 

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. 

Vitamin D is a precursor for a number of compounds that increase intestinal absorption and decrease renal excretion of calcium and phosphate. Metabolites of vitamin D and their pharmacologic analogs are typically used to increase blood calcium and phosphate levels and to enhance bone mineralization in conditions such as osteodystrophy, rickets, or other situations where people lack adequate amounts of vitamin D. Vitamin D analogs such as calcitriol have also been combined with calcium supplements to help treat postmenopausal osteoporosis,4,9 and to treat bone loss caused by antiinflammatory steroids (glucocorticoids see Chapter 29 28.76 Specific vitamin D-related compounds and their clinical applications are listed in Table 31-5. 

A number of factors have been shown to alter the rate of excretion of chromium in humans. Intravenous injection of calcium EDTA resulted in a rapid increase in the urinary excretion of chromium in metal workers (Sata et al. 1998). Both acute and chronic exercises have been shown to increase chromium excretion in the urine, though the increased excretion did not appear to be accompanied with decreased levels of total native chromium (Rubin et al. 1998). An increased rate of chromium excretion has been reported in women in the first 26 weeks of pregnancy (Morris et al. 1995b). Chromium supplementation did not appear to alter the rate of excretion into breast milk in postpartum women (Mohamedshah et al. 

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,...

Although it might seem reasonable to treat osteoporosis with vitamin D, it must be realized that the primary funebon of vitamin D is to maintain plasma calcium levels, not to promote bone formation. An end-effect of vitamin D supplementa-hon is an increase in bone resorpbon and increased excretion of calcium in the urine. Calcium supplements should not be used indiscriminately Two types of persons should not receive calcium supplements persons with hypercalcemia and persons with kidney stones or a family history of kidney stones. These two issues are discussed in the following pages. 

Stone formation may occur in those with elevated levels of urinary calcium, Mormally adults excrctc less than 200 mg of calcium in the urine per day, even with relatively high intakes of calcium, A fraction of the population absorbs more calcium than normal and excretes more calcium in the urine, resulting in hyper-calciuria. Hypercalciuria is defined as urinary excretion of calcium of more than 300 mg/day. About half of patients with calcium stones have hypercalciuria and may be calcium hyper absorbers. Persons with hypercalciuria are advised to limit their calcium intake to one serving of milk or cheese per day. They are also advised to limit their protein intake to the RDA. Their protein intake should be limited to minimize the caiciuric effect of protein. They are also advised to fnerense their water intake to produce 2 liters of urine per day and to avoid oxalate-containing foods. Persons with hypercalciuria and with a familial history of stones should not lake calcium supplements to raise their intake above the RDA. 

Hypoparathyroidism can result from decreased production of PTH or failure of target organs to respond to PTH. In rare cases, it involves the production of genetically defective PTH. PTH provokes the kidney to conserve calcium and to excrete phosphate. Thus, hypoparathyroidism results in low plasma calcium and high plasma phosphate levels. The disease may result in the calcification of soft tissues because of the high plasma phosphate level. Elevated phosphate levels result in an increased rate of precipitation of calcium and phosphate as the calcium phosphate salt. The disease is treated with oral calcium supplements and phosphate-binding antacids to minimize the absorption of dietary phosphate. 

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