section 37.1
Calcium and Phosphorus
o f the occurrence o f osteoporosis. A dm inistration o f vita-
m in D m etabolites together w ith the calcium is indicated
for older w om en.
M ajor dietary sources o f calcium are m ilk and dairy
products, such as ch eese and yogurt. C ow ’s m ilk contains
120 m g o f C a2+ per deciliter (30 m m ol/L ) and is now usu-
ally supplem ented w ith vitam in D . Sardines (and other
sm all fish w h ose bones are consum ed) and soybean prod-
ucts can provide significant am ounts o f calcium . Soybean
curd, know n as tofu and eaten w id ely in C hina and Japan,
contains 128 m g o f Ca2+ per 100 g. Dark green leafy v eg -
etables, legum es, nuts, and w hole-grain cereal products
contribute to dietary calcium .
W hen the recom m ended daily allow ance (R D A ) for cal-
cium is not m et by the diet is (particularly in w om en), sup-
plem entation in the form o f calcium salts is recom m ended.
C alcium salts vary w id ely in calcium content; by w eight,
calcium gluconate has 9% , calcium lactate has 13%, and
calcium carbonate has 40% calcium . A bsorption o f cal-
cium from salts m ay vary; calcium carbonate is the m ost
poorly absorbed. B on e m eal and dolom ite are not recom -
m ended sources o f calcium , since they m ay contain lead,
arsenic, mercury, and other toxic m etals. A potential com -
plication o f excessive calcium intake is form ation o f uri-
nary tract stones; this risk m ay be reduced by am ple fluid
C alcium
throughout the sm all intestine and, to a sm all extent, in
the colon. The active transcellular transport occurs in
the duodenum and the passive paracellular process takes
place in the jejunum and ileum . T he chem ical gradient
and the sojourn tim e o f the food passing through the intes-
tine determ ine the m ovem ent o f calcium that occurs by a
passive process. The absorption o f calcium in the colon b e-
com es nutritionally significant under conditions o f sm all
intestine resection.
The active, saturable calcium transport con sists o f three
steps: uptake by the brush-border cell m em brane, diffusion
through the cytoplasm , and extrusion at the basolateral
surface w here calcium is transferred to the portal blood
circulation. The first step o f calcium uptake is not energy-
dependent, the second step o f transcellular calcium m ove-
m ent is thought to be a rate-lim iting process, and third
step o f calcium extrusion from the enterocyte is an energy-
dependent process. The energy-dependent process is m e-
diated by Ca
+ -ATPase, w hich form s a transmembrane
segm ent, and the en zym e undergoes phosphorylation-
induced conform ational changes. This transcellular ac-
tive calcium transport requires la,25-d ih ydroxyvitam in
D [l,2 5 -(O H )2 D , calcitriol], w hich is responsible for
inducing the synthesis o f enterocyte calcium -binding
prom ote
m ovem ent as w ell as enhancing the num ber o f Ca2+-
ATPase pum ps. Increased p hysiological need during preg-
nancy, lactation, and growth enhances calcium absorption.
The m olecular m echanism by w hich this occurs is not un-
Phosphate is also absorbed in the sm all intestine by
an active process, with m axim al absorption occurring in
the m iddle o f the jejunum . l,25-(O H )2D also m ediates
phosphate absorption.
Intestinal calcium absorption is influenced by dietary
factors. L actose and other sugars increase water absorp-
tion, thereby enhancing passive calcium uptake. The effect
o f lactose is especially valuable because o f its presence in
m ilk, a major source o f calcium . L actose also increases
absorption o f other m etal ions. This effect m ay contribute
to the incidence o f lead p oisoning (plum bism ) am ong
young inner-city children exp osed to high dietary levels
o f both lead and lactose.
C alcium absorption is reduced by high pH; com plex-
ing agents such as oxalate, phytate, free fatty acids, and
phosphate; and shortened transit tim es. T hese factors are
probably o f clinical im portance on ly w hen associated
w ith vitam in D deficiency, m arginal calcium intake, or
m alabsorption disorders. A bsorption is also reduced by
increased intake o f protein, fat, and plant fiber; increas-
ing age; stress; chronic alcoholism ; im m obilization (e.g.,
prolonged hospitalization); and drugs such as tetracy-
cline, thyroid extract, diuretics, and alum inum -containing
A s intestinal absorption o f calcium increases, urinary
calcium excretion also increases. W hen the latter exceeds
300 m g/d, form ation o f calcium phosphate or calcium o x -
alate stones (
) m ay occur. H ypercalciuria m ay
result from decreased reabsorption o f calcium due to a
renal tubular defect or from increased intestinal absorp-
tion o f calcium . H ypercalciuria m ay be due to an intrinsic
defect in the intestinal m ucosa or secondary to increased
synthesis o f l,2 5 -(O H )2D in the kidney. D isordered regu-
lation o f l,2 5 -(O H )2D synthesis is relatively com m on in
idiopathic hypercalciuria. Treatment usually includes re-
duction in dietary calcium . Increased vitam in D intake,
hyperparathyroidism , and other disorders can also cause
hypercalciuria and urolithiasis.
In som e form s o f steatorrhea, calcium , w hich norm ally
binds to and precipitates oxalate in the intestine, binds
instead to fatty acids producing increased oxalate absorp-
tion and hyperoxaluria. E ven though urinary calcium is
decreased under these conditions, the concentration o f uri-
nary oxalate m ay be elevated sufficiently to cause precip-
itation o f calcium oxalate crystals. Stone form ation can
be exacerbated by a diet that contains foods rich in o x -
alate, such as rhubarb, citrus fruits, tea, and cola drinks.
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