الفهرس 
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Abstract
The maintenance of calcium homeostasis is very important because calcium is the main component of bony skeleton and serves as the intracellular and extracellular messenger in numerous essential cellular events. This is achieved by harmony between the intestine (the place for calcium absorption), the bone (the main storage place for calcium), and the kidney (the main place of elimination of the absorbed calcium). Most of the serum calcium filtered by the glomerulus (>60%) is reabsorbed in the proximal tubule. This is accomplished by a paracellular pathway involved tight junction proteins claudins-2 and -12. This process is driven by water and particularly sodium reabsorption. About 20% to 25% of the remaining calcium is reabsorbed in the thick ascending limb of Henle using a similar mechanism. The distal convoluted tubule and the collecting ducts regulate the remaining calcium excretion and reabsorption. Defects in this pathway may cause excessive excretion of calcium in the urine leading to hypercalciuria. Calcium homeostasis depends on calcium absorption and excretion. Calcium absorption is dependent on calcium intake, vitamin D status and calcium phosphors ratio (Ca/P ratio). Formula milk has higher concentrations of calcium and phosphorus but with lower bio‐availabilities of both nutrients compared with human milk. The Ca/P ratio may be an important determinant of calcium absorption and retention. In breast milk, the Ca/P ratio is approximately 2:1, with similar ratios in infant formulas; however, absolute quantities are higher in infant formulas to account for the differing bioavailabilities. Vitamin D supplementation is known to increase UCa/Cr in vitamin D deficient children and adolescents. However, UCa/Cr is not affected in vitamin D sufficient children and adolescents. Hence, vitamin D status is an important determinant of UCa/Cr. If calcium absorption is inadequate, serum parathyroid hormone (PTH) rises and calcium homeostasis is maintained by altered bone resorption and renal calcium excretion. The urinary excretion of calcium has been evaluated by assessing the quantity of calcium in a 24-hour urine collection, but assessment of UCa excretion by expression of the urinary concentration of calcium in relation to creatinine (UCa/Cr) in spot urine samples is well suited for infants in whom 24-hour urine collections are difficult to obtain. So, Calcium/creatinine ratio is considered a screening test used to detect the presence of disorders that lead to excess calcium in the urine. The UCa/Cr is higher in infants than in older children and adults, and steadily diminishes with age until the value of 0.21 mg/mg. this may be due to decreased creatinine excretion in infants, Since creatinine is derived from creatine in muscle, its urinary excretion is dependent on the muscle mass of the subject. Dietary habits can have a significant impact on calcium handling by the renal tubules. Urinary calcium excretion is significantly affected by sodium, protein, potassium, phosphorous, and calcium in the diet. An increase in either oral or intravenous sodium chloride inhibits net renal tubular calcium absorption and is used with beneficial effect in the treatment of hypercalcemia to increase urinary calcium excretion. Thus, a diet high in sodium can lead to hypercalciuria. Also, an increase in dietary protein intake increases net acid excretion because of the release of protons from oxidation of sulfur in the amino acids methionine, cysteine, and cystine. Urine calcium excretion increases as net acid excretion increases; hence, it rises progressively as the protein intake increases. Many other factors, such as ethnicity, genetics and sun exposure can have an impact on calcium excretion. All of these factors are modulated in infancy by feeding choices during the first months of life, when the infant’s diet is predominantly comprised of milk. So, we aimed to investigate calcium excretion in healthy infants at ages ranging from 2 to 6 months according to their feeding either breast or artificial milk. Infant formula is an effective substitute to breast milk and is formulated to mimic the nutritional composition of breast milk. Although production of an identical product to breast milk is not feasible, every effort has been taken to mimic the nutrition profile of human breast milk for normal infant growth and development. If infants are not breastfed, commercial infant formula is the only appropriate food for 6 months until infants start solid foods. Infant formula use should continue until at least 12 months of age, when infants can transition to cow’s or other calcium‐rich milks. By comparison artificial milk has higher levels of fat, minerals and protein than breast milk. Apparently 80 healthy full term infants were eligible for participation in the study. Forty of them were exclusively breast fed and the other forty were exclusively artificial fed. Infants were enrolled at age ranging from two to six months. Infants with known kidney disorders, failure to thrive, any syndromatic facies or who were on mixed feeding were excluded from the study. This study was done after informed consent from the parents. Demographic data and anthropometric measurements of both groups were recorded. Formula-fed infants were randomized to receive different types of formula and formula compositions were recorded. A blood sample was drawn and spot morning urinary sample was taken from all Participants. Renal Ultrasonography was performed for exclusion of renal anomalies.