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chapter 37
Mineral Metabolism
TABLE 37-1
Factors That Can Influence Calcium and Phosphate Homeostasis
Factor
Pathological Effects on Calcium
and Phosphorous Metabolism*
Mechanism/Site of Action^
V itam in D
E xcess (vitam in D toxicosis) causes
hypercalciuria and hypercalcem ia,
leading to urolithiasis and soft-
tissue (esp ecially renal)
calcification; insufficiency causes
rickets and osteoporosis.
A s l,2 5 -(O H )2D , increases bone
resorption and intestinal and
renal C a2+ and phosphate
absorption; other m etabolites
m ay have other activities,
especially in bone.
Parathyroid horm one (PTH )
Primary hyperparathyroidism
causes hypercalcem ia,
hypophosphatem ia, and increased
urinary cA M P; hypoparathyroidism
causes h ypocalcem ia and
hyperphosphatem ia, often with
soft-tissue calcification and tetany
and convulsions.
B inds to cell-surface receptors
and activates adenylate cyclase;
increases bone m ineralization
and activity o f renal l a -
hydroxylase; in kidney,
reabsorption o f Ca2+ increases
and reabsorption o f phosphate
decreases.
Parathyroid horm one-
related protein (PTHrP)
Predom inant factor responsible for
hypercalcem ia o f m alignancy.
PTHrP functions through the
activation o f PTH receptor;
it has paracrine functions, it
regulates rate o f cartilage
differentiation and increase
placental calcium transport, it
m ay also have PTHrP specific
receptors.
C alcitonin
N either d eficiency nor ex cess o f
calcitonin is known to have any
pathological effects. Plasm a
calcitonin is increased in the
m edullary carcinom a o f the
thyroid.
B inds to cell-surface receptors
in bone and kidney, increasing
intracellular cA M P; m ay also
function by activation o f
phospholipase C signal
transduction pathway, decreases
C a2+ release from bone and
stim ulate Ca2+ and phosphate
excretion in kidneys, generally
antagonistic to PTH.
M agnesium
H yperm agnesem ia decreases PTH
secretion; m ild hypom agnesem ia
increases PTH secretion; severe
hypom agnesem ia (<0.05m m ol/L )
inhibits PTH secretion, even with
hypocalcem ia.
N eeded to maintain parathyroid
responsiveness to serum Ca2+.
(continued)
