The Changing Role of Sodium Management in Cirrhosis

Opinion Statement Hyponatremia may occur in patients with cirrhosis and ascites mainly due to water retention and an inability of the kidney to excrete free water. The main reason for this abnormality is related to the fact that these patients have portal hypertension and this leads to systemic vaso...

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Bibliographic Details
Published in:Current treatment options in gastroenterology 2016-06, Vol.14 (2), p.274-284
Main Authors: Lizaola, Blanca, Bonder, Alan, Tapper, Elliot B., Mendez-Bocanegra, Angela, Cardenas, Andres
Format: Article
Language:English
Subjects:
Gastroenterology
Liver (J Bajaj
Medicine
Medicine & Public Health
Section Editor
Topical Collection on Liver
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Summary:Opinion Statement Hyponatremia may occur in patients with cirrhosis and ascites mainly due to water retention and an inability of the kidney to excrete free water. The main reason for this abnormality is related to the fact that these patients have portal hypertension and this leads to systemic vasodilation that in turn activates sodium-retaining and water-retaining systems such as the renin-angiotensin-aldosterone system and arginine vasopressin (AVP). AVP increases solute-free water retention by acting on the V2 receptors of the kidney-collecting tubes. Hyponatremia in cirrhosis is defined as a serum sodium level less than 130 meq/L. The appearance of hyponatremia in patients with advanced cirrhosis portends a poor prognosis before and after liver transplantation. Treatment of hyponatremia is difficult; fluid restriction rarely increases serum sodium levels and other therapies are associated with important drawbacks. A thorough discussion of the underlying mechanisms leading to hyponatremia and hypernatremia in cirrhosis and current treatment options including the use of vaptans (V2 receptor antagonists) are discussed in this review.
ISSN:1092-8472
1534-309X
DOI:10.1007/s11938-016-0094-y