Calcium Metabolism in Health and Disease | American Society of Nephrology

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Figure 1.
(A) Calcium transport in women and girls. Gut absorption, bone deposition, bone resorption, and bone retention were significantly lower, whereas urinary excretion was significantly higher in women (n = 11; mean age, 22 yr) versus girls (n = 14; mean age, 13 yr) (12). (B) Racial differences in calcium transport in American girls. Bone deposition and bone retention were significantly lower, whereas urinary excretion was significantly higher in white girls (n = 14; mean age, 13.7 yr) versus black girls (n = 14; mean age, 12.8 yr). Values are mean ± SD (mg/d). *Significant difference in mean values (14).
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Figure 2.
Regulation of serum calcium homeostasis. Serum calcium homeostasis is regulated by a rapid negative feedback hormonal pathway involving the concentration of ionized calcium in serum (Ca, green arrows) and the secretion of parathyroid hormone (PTH, blue arrows) from the parathyroid. A fall in serum calcium (↓ Ca) inactivates the calcium receptor in the parathyroid cell (CaR; green circle) and increases PTH secretion (↑ PTH), which restores serum calcium (↑ Ca) by activating the parathyroid receptor (PTHR; blue circles) in bone, to increase calcium resorption, and in kidney, to increase tubular calcium reabsorption. In kidney, the increased PTH secretion augments its calcium-restorative effect by increasing secretion of 1,25-dihydroxyvitamin D (1,25D; red arrows), which, acting on the vitamin D receptor (VDR, red circles) in gut, increases active calcium absorption and increases calcium resorption in bone.
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Figure 3.
Regulation of serum phosphate (P) homeostasis: interface with serum calcium (Ca) homeostasis at the kidney. Serum phosphate homeostasis is regulated by a negative feedback hormonal pathway (black arrows) involving the concentration of phosphate in serum (P, blue square) and the secretion of fibroblast growth factor 23 (FGF-23; blue circles) from bone cells. A fall in serum P (↓) decreases secretion of FGF-23 (↓), which restores serum P by acting on the type 2 sodium-phosphate renal tubular transporters (NaPi-II) to increase (↑) phosphate reabsorption (TmP; red squares) and by increasing secretion (↑) of renal 1,25-dihydroxyvitamin D (1,25D; purple hexagons) to increase phosphate gut absorption. A rise (↑) in serum P increases (↑) FGF-23 secretion, which restores serum P by lowering (↓) phosphate reabsorption (TmP; red squares) and by lowering secretion (↓) of renal 1,25-dihydroxyvitamin D (1,25D; purple hexagons) to decrease phosphate gut absorption. Changes in the Ca–PTH homeostatic system also have major effects on serum P, but not through a negative feedback pathway, because serum P does not directly regulate PTH secretion. Ca-induced changes in PTH secretion (green circles) induce changes in serum P by regulating tubular phosphate reabsorption (TmP; red squares) through the activity of the NaPi-ll renal tubular transporters. It should be noted that, although both FGF-23 and PTH have the same action on renal tubular reabsorption (TmP; red squares), these hormones have opposing effects on renal 1,25-dihydroxyvitamin D (1,25D; purple hexagons) secretion; the P-FGF23 homeostatic system is more slowly acting than the Ca-PTH homeostatic system; and the receptor for serum P remains to be discovered.