ai T3 C

Calcium and Phosphate Metabolism

Calcium, particularly ionized calcium (Ca2+), plays a central role in the regulation of numerous cell functions (^ pp.36, 62ff., 192, 276). Calcium accounts for 2% of the body weight. Ca. 99% of the calcium occurs in bone while 1% is dissolved in body fluids. The total calcium conc. in serum is normally 2.1-2.6 mmol/L. Ca. 50% of it is free Ca2+ (1.1-1.3 mmol/L) while ca. 10% is bound in complexes and 40% is bound to proteins (mainly albumin; ^ p. 178). Calcium protein binding increases as the pH of the blood rises since the number of Ca2+ binding sites on protein molecules also rises with the pH. The Ca2+ conc. accordingly decreases in al-kalosis and rises in acidosis (by about 0.21 mmol/L Ca2+ per pH unit). Alkalosis (e.g., due to hyperventilation) and hypocalcemia (see below) can therefore lead to tetany.

The calcium metabolism is tightly regulated to ensure a balanced intake and excretion of Ca2+ (^ A). The dietary intake of Ca2+ provides around 12-35 mmol of Ca 2+ each day (1 mmol = 2 mEq = 40 mg). Milk, cheese, eggs and "hard" water are particularly rich in Ca2+. When calcium homeostasis is maintained, most of the ingested Ca2+ is excreted in the feces, while the remainder is excreted in the urine (^ p. 178). When a calcium deficiency exists, up to 90% of the ingested Ca2+ is absorbed by the intestinal tract (^ A and p. 262).

Pregnant and nursing mothers have higher Ca2+ requirements because they must also supply the fetus or newborn infant with calcium. The fetus receives ca. 625 miTiol/day of Ca2+ via the placenta, and nursed infants receive up to 2000 mmol/day via the breast milk. In both cases, the Ca2+ is used for bone formation. Thus, many women develop a Ca2+ deficiency during or after pregnancy.

Phosphate metabolism is closely related to calcium metabolism but is less tightly controlled. The daily intake of phosphate is about 1.4 g; 0.9 g of intake is absorbed and usually excreted by the kidneys (^ p. 178). The phosphate concentration in serum normally ranges from 0.8-1.4 mmol/L.

Calcium phosphate salts are sparingly soluble. When the product of Ca2+ conc. times phosphate conc. (solubility product) exceeds a certain threshold, calcium phosphate starts to precipitate in solutions, and the deposition of calcium phosphate salts occurs. The salts are chiefly deposited in the bone, but can also precipitate in other organs. The infusion of phosphate leads to a decrease in the serum calcium concentration since calcium phosphate accumulates in bone. Conversely, hypo-phosphatemia leads to hypercalcemia (Ca2+ is released from bone).

Hormonal control. Calcium and phosphate homeostasis is predominantly regulated by parathyroid hormone and calcitriol, but also by calcitonin to a lesser degree. These hormones mainly affect three organs: the intestines, the kidneys and the bone (^ B and D).

Parathyrin or parathyroid hormone (PTH) is a peptide hormone (84 AA) secreted by the parathyroid glands. Ca2+ sensors in cells of the parathyroid glands regulate PTH synthesis and secretion in response to changes in the plasma concentration of ionized Ca2+ (^ p. 36). More PTH is secreted into the bloodstream whenever the Ca2+ conc. falls below normal (hypocalcemia). Inversely, PTH secretion decreases when the Ca2+ level rises (^ D, left panel). The primary function of PTH is to normalize decreased Ca2* conc. in the blood (^ D). This is accomplished as follows: (1) PTH activates osteoclasts, resulting in bone breakdown and the release of Ca2+ (and phosphate) from the bone; (2) PTH accelerates the final step of calcitriol synthesis in the kidney, resulting in increased reabsorption ofCa2+ from the gut; (3) in the kidney, PTH increases calcitriol synthesis and Ca2+ reabsorption, which is particularly important due to the increased Ca2+ supply resulting from actions (1) and (2). PTH also inhibits renal phosphate reabsorption (^ p. 178), resulting in hypophosphatemia. This, in turn, stimulates the release of Ca2+ from the bone or prevents the precipitation of calcium phosphate in tissue (solubility product; see above).

Hypocalcemia occurs due to a deficiency (hypoparathyroidism) or lack of efficiency (pseudohypoparathyroidism) of PTH, which can destabilize the resting potential enough to produce muscle spasms and tetany. These deficiencies can also lead to a secondary calcitriol deficiency. An excess of PTH (hyperparathyroidism) and malignant osteolysis overpower the Ca2+ control mechanisms, leading to hypercalcemia. The long-term elevation of Ca2+ results in cal-

iā€” A. Calcium metabolism

Milk, cheese, eggs and hard water

Milk, cheese, eggs and hard water


in feces

18mmol/day (at an intake of 20 mmol/day)

B. Factors affecting the blood Ca2+ concentration



|ā€” C. Calcitriol synthesis

UV light

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