C h a p t e r 8
Disorders of Fluid, Electrolyte, and Acid–Base Balance
187
the condition leads to joint stiffness, bone pain, and
skeletal deformities consistent with osteomalacia (see
Chapter 44).
Treatment.
The treatment of hypophosphatemia is
usually directed toward prophylaxis. This may be
accomplished with dietary sources high in phosphorus
(one glass of milk contains approximately 250 mg of
phosphorus) or with oral or intravenous replacement
solutions. Phosphorus supplements usually are contra-
indicated in hyperparathyroidism, chronic kidney dis-
ease, and hypercalcemia because of the increased risk of
extracellular calcifications.
Hyperphosphatemia
Hyperphosphatemia represents a serum phosphorus
concentration in excess of 4.5 mg/dL (1.45 mmol/L) in
adults. Moderate hyperphosphatemia exists when serum
phosphate is in the range of 4.6 to 6.0 mg/dL (1.49 to
1.94 mmol/L) and severe phosphatemia when serum
phosphate levels are greater than 6.0 (1.94 mmol/L).
3
Hyperphosphatemia can result from failure of the
kidneys to excrete excess phosphate, rapid redistri-
bution of intracellular phosphate to the ECF com-
partment, or high phosphate intake.
3,45
Because
phosphorus is primarily eliminated by the kidneys,
hyperphosphatemia due to impaired renal function
is a common electrolyte disorder in persons with
chronic kidney disease
3,46
(see Chapter 26). Release of
intracellular phosphorus can result from conditions
such as massive tissue injury, rhabdomyolysis (muscle
dissolution), heat stroke, potassium deficiency, and
seizures. The administration of excess phosphate-containing antacids, laxatives, or enemas can be
another cause of hyperphosphatemia, especially when
there is a decrease in vascular volume and a reduced
glomerular filtration rate. Phosphate-containing laxa-
tives and enemas predispose to hypovolemia and a
decreased glomerular filtration rate by inducing diar-
rhea, thereby increasing the risk of hyperphosphate-
mia. Serious and even fatal hyperphosphatemia has
reportedly resulted from administration of phosphate
enemas.
47
Manifestations.
Many of the signs and symptoms
of a phosphate excess are related to a calcium deficit
(see Table 8-7). Because of the reciprocal relationship
between calcium and phosphorus levels, a high serum
phosphate level tends to lower serum calcium levels,
which can lead to tetany and other signs of hypocal-
cemia.
3
Inadequately treated hyperphosphatemia in
chronic kidney disease can lead to renal bone disease,
and extraosseous calcifications in soft tissues (see
Chapter 26). A secondary effect of hyperphosphate-
mia in chronic kidney disease is stimulation of nodular
hyperplasia of the parathyroid glands that results in a
secondary hyperparathyroidism.
46
Treatment.
The treatment of hyperphosphatemia is
directed at the cause of the disorder. Dietary restriction
of foods that are high in phosphorus may be used.
Calcium-based phosphate binders are useful in chronic
hyperphosphatemia. Sevelamer, a recently approved
calcium- and aluminum-free phosphate binder, is as
effective as a calcium-based binder, but lacks its adverse
effects.
3
Hemodialysis is used to reduce phosphate levels
in persons with chronic kidney disease.
Disorders of Magnesium Balance
Magnesium is the second most abundant intracellular
divalent cation.
48–50
Although the average adult has
approximately 24 g of magnesium distributed through-
out the body, only an estimated 2% is distributed in the
ECF.
50,51
The normal serum concentration of magnesium
is 1.3 to 2.1 mg/dL (0.65 to 1.1 mmol/L).
3
Regulation of Magnesium Balance
Magnesium is ingested in the diet, absorbed from the
intestine, and excreted by the kidneys. Intestinal absorp-
tion is not closely regulated, and only about 30% to
50% of dietary magnesium is absorbed.
48
The kidney
is the principal organ of magnesium regulation. The
kidneys filter about 80% of the serum magnesium and
only about 3% is excreted in the urine, although this
amount can be influenced by other conditions and medi-
cations.
48
Renal reabsorption is stimulated by PTH and
is decreased in the presence of increased serum levels of
magnesium and calcium.
Magnesium is a cofactor in hundreds of metabolic
reactions in the body. It is required for cellular energy
metabolism, functioning of the Na
+
/K
+
-ATPase mem-
brane pump, membrane stabilization, nerve conduction,
and ion transport. It also acts as a cofactor in many
intracellular enzyme reactions, including the transfer of
high-energy phosphate groups in the generation of ATP
from adenosine diphosphate (ADP). It is essential to all
reactions that require ATP, for every step related to rep-
lication and transcription of DNA, and for translation
of messenger RNA.
3,48–50
Magnesium also participates in potassium and cal-
cium channel activity. Magnesium blocks the outward
movement of potassium in cardiac cells, preventing
the development of cardiac arrhythmias.
51
It also acts
as a smooth muscle relaxant by altering calcium levels
that are responsible for muscle contraction. Because
of its smooth muscle relaxing effect, there has been a
recent interest in the use of magnesium in the treatment
of severe bronchial asthma.
56
In addition, it has been
suggested that magnesium may have an anticonvulsant
effect. Currently, it is the first-line drug in the prevention
and treatment of seizures associated with eclampsia in
pregnant women (see Chapter 18).
52
Hypomagnesemia
Magnesium deficiency refers to depletion of total body
stores and hypomagnesemia to a low serum concentra-
tion of less than 1.3 mg/dL (0.65 mmol/L).
3
It is seen
in conditions that limit intake or increase intestinal or
