Abstract
Background
Rhabdomyolysis is an uncommon complication of hyponatremia, reported previously only
in case reports and small retrospective studies, and its underlying mechanism is controversial.
Some studies support the hypothesis that the rapid correction of hyponatremia is responsible
for rhabdomyolysis, whereas others emphasize the severity of the hyponatremia as a
predisposing factor for rhabdomyolysis.
Objectives
To test the association between hyponatremia and rhabdomyolysis and to demonstrate
a causal association.
Methods
Hyponatremia was induced by administration of water and desmopressin acetate in rats
during 3 days, followed by its rapid correction, using animal models established for
the evaluation of central pontine myelinolysis. The plasma creatine phosphokinase
levels, a marker for rhabdomyolysis, were monitored, and hematoxylin and eosin sections
of the quadriceps and gastrocnemius muscles were evaluated for signs of rhabdomyolysis.
Results
The induction of hyponatremia and its correction were accompanied by the previously
reported neurological sequelae, including signs of central pontine myelinolysis. However,
no increase in plasma creatine phosphokinase levels was found, and histopathological
examination of the quadriceps and gastrocnemius muscles revealed no sign of rhabdomyolysis.
Conclusions
The present study, which is the first to test the association between hyponatremia
and rhabdomyolysis in an animal model, does not support any causal association between
hyponatremia and rhabdomyolysis. Thus, other factors might be necessary for an association
between hyponatremia and rhabdomyolysis, such as genetic factors or convulsions that
are known to be associated with both hyponatremia and rhabdomyolysis. Further research
in this important physiologic and clinical question is needed.
Keywords
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Article info
Publication history
Published online: February 03, 2014
Accepted:
August 16,
2013
Received in revised form:
July 13,
2013
Received:
February 17,
2013
Identification
Copyright
© 2014 Elsevier Inc. Published by Elsevier Inc. All rights reserved.
