Page 136 - Color Atlas Of Pathophysiology (S Silbernagl Et Al, Thieme 2000)

Abnormalities of Magnesium Balance
Half of the body’s magnesium is bound in Even when the Mg 2+ balance is in equilib-
bone, almost one half is intracellular. Mg 2+ rium shifts of Mg 2+ between the intracellular
concentration in extracellular fluid is relative- and extracellular spaces can change the plas-
2+
ly low (≈ 1 mmol/L). Mg 2+ is essential for the ma concentration of Mg . As insulin stimu-
+
activity of numerous enzymes. In many func- lates the cellular uptake of both K (→ p.124)
2+
tions it acts antagonistically to Ca , which it and Mg 2+ (→ A3, A7), loss of Mg 2+ may occur
can displace from its binding to proteins. In in diabetes mellitus or prolonged fasting. Sub-
can inhibit the release of trans-
this way Mg 2+ 2+ as it has been shown for K that stitution of insulin or resumption of food in-
Kidney, Salt and Water Balance the plasma concentration measured in a blood from the damaged pancreas split triglycerides
take may then bring about hypomagnesemia.
mitters in synapses of the nervous system and
2+
can thus inhibit synaptic transmission. It is as
may occur in
A decrease in ionized Mg
+
true for Mg
acute pancreatitis (→ A4). Activated lipases
(TGs) in the fat tissue, and the liberated fatty
sample is an unreliable indicator of its real
2+
concentration.
acids (FAs) together with Mg
form insoluble
Magnesium deficiency occurs when there is
complexes (Mg[FA] 2 ).
2+ deficiency are an in-
The effects of Mg
an inadequate supply or a loss via the gut (mal-
absorption; → A1; see also p.152ff.) or the kid-
creased neuromuscular excitability, hyperre-
sometimes resemble those after damage to
absorbed in the ascending part of the loop of
Henle (→ p. 96). Its reabsorption takes place
the basal ganglia (→ p. 312ff.). Cardiovascular
paracellularly through the tight junctions,
signs can be tachycardia and arrhythmias,
5 neys. In the kidneys magnesium is mainly re- flexia, and cramps (→ A5). These cramps
driven by the transepithelial potential that is even ventricular fibrillation, and a rise in blood
indirectly created by NaCl reabsorption pressure. These symptoms are accentuated (if
(→ A2). The permeability of the tight junctions not in fact caused by) hypercalcemia that may
is reduced in hypercalcemia and alkalosis. This occur as a result of a decreased release of PTH
results, for example, in magnesuria. In a rare (Mg 2+ stimulates the release of PTH). Usually
genetic disease, the protein allowing for para- Mg 2+ deficiency coexists with K + deficiency
cellular transport (paracellin) is defective. The (common causes; → p.124) so that the symp-
most prominent disorder of those patients is toms of hypokalemia are accentuated.
magnesuria. Furthermore, Ca 2+ inhibits, via a Mg 2+ excess is caused by renal failure
+
–
+
Ca 2+ receptor, Na -K -2 Cl cotransport, caus- (→ A6). If the glomerular filtration rate is re-
ing a decrease in the transepithelial potential duced (GFR↓), Mg 2+ excretion can at first be
and thus of Mg 2+ reabsorption. A genetic de- maintained by a reduction in reabsorption.
–
+
+
fect of the Na -K -2 Cl cotransporter, of the Only if GFR drops below ca. 30 mL/min can a
–
+
Cl channel or of the luminal K channel (Bart- decrease of filtration no longer be compensat-
ter’s syndrome) similarly leads to magnesuria. ed by the tubules. Hypermagnesemia (without
2+
NaCl reabsorption and thus the transepithe- excess Mg ) can also occur in diabetes mellitus
2+
lial potential in the ascending limb are in- (→ A7). Lastly, excessive supply of Mg 2+ (Mg -
creased by ADH. ADH release ceases in alcohol- containing infusions, parenteral feeding, or
ism, and the reabsorption of NaCl and Mg 2+ therapeutic Mg 2+ administration to reduce
falls. neuromuscular excitability) can cause hyper-
The reabsorption of Mg 2+ is also reduced in magnesemia.
salt-losing nephropathy, in osmotic diuresis The effects of Mg 2+ excess are impaired
(e.g., glycosuria in diabetes mellitus), and due neuromuscular excitability (hyporeflexia) that
to the effect of loop diuretics. Renal loss of may even lead to respiratory arrest, disorders
Mg 2+ also occurs in hyperaldosteronism, prob- of cardiac action potential generation and
ably via volume expansion, which causes re- propagation, vomiting, and constipation (→
+
duced Na and Mg 2+ reabsorption in the prox- A8).
126 imal tubules and the ascending limb (→ A2).
Silbernagl/Lang, Color Atlas of Pathophysiology © 2000 Thieme
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