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Hyponatremia

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Hyponatremia
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.
Although the definition may vary among different clinical laboratories, hyponatremia is commonly defined as a serum sodium concentration ≤135 meq/L [2]. An overview of the causes of hyponatremia will be presented here (table 1). Most of the individual disorders are discussed in detail separately, as are issues related to diagnosis and treatment [1,3]. (See "Diagnosis of hyponatremia" and "Overview of the 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 "Hyponatremia in heart failure".)
DISORDERS

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