Ionized calcium in the plasma is freely filtered by the kidney so that very large amounts enter the kidney each day, but 99.8% of this calcium is reabsorbed throughout the nephron. Regulated active transport occurs in the distal convoluted tubule and involves vitamin D, CaBP, and PTH. Typically, approximately 2.5-6 mmol (100-240 mg) of calcium is excreted in urine daily.

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 100mmol (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.

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