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Burton D Rose, MD
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INTRODUCTION In almost all cases, hyponatremia results from the
intake (either oral or intravenous) and subsequent retention of water [ 1].
A water load will, in normal subjects, be rapidly excreted as the dilutional
fall in plasma osmolality suppresses the release of antidiuretic hormone
(ADH), thereby allowing the excretion of a dilute urine. The maximum
rate of water excretion on a regular diet is over 10 liters per day, thereby
providing an enormous range of protection against the development of
hyponatremia.
Some patients with primary polydipsia retain water and become
hyponatremic because they drink such large quantities of fluid that they
overwhelm the excretory capacity of the kidney. In almost all cases,
however, hyponatremia occurs because there is an impairment in renal
water excretion, due most often to an inability to suppress ADH release.
An overview of the causes of hyponatremia will be presented here ( show
table 1); most of the individual disorders are discussed in detail
separately, as are issues in diagnosis and treatment [ 1]. ( See "Diagnosis
of hyponatremia" and see "Treatment of hyponatremia").
It should also be emphasized that, in selected patients, multiple factors
may contribute to the fall in the plasma sodium concentration.
Symptomatic infection with human immunodeficiency virus (HIV) is an
example of this phenomenon, as volume depletion, the syndrome of
inappropriate ADH secretion, and adrenal insufficiency all may be present.
( See "Electrolyte disturbances with HIV infection").
The presence of hyponatremia, even of relatively mild severity, is
associated with adverse survival. This includes patients with heart and/or
hepatic failure, and/or acute myocardial infarction. ( See "Hyponatremia
in cirrhosis" and see "Hyponatremia in heart failure").
DISORDERS IN WHICH ADH LEVELS ARE ELEVATED The two most
common causes of hyponatremia are effective circulating volume
depletion and the syndrome of inappropriate ADH secretion, disorders in
which ADH secretion is not suppressed.
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31. Thaler, SM, Teitelbaum, I, Berl, T. "Beer potomania" in non-beer
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