REVIEW ARTICLE Hyponatremia in patients with liver diseases: not just a cirrhosis-induced hemodynamic compromise G. Liamis 1 • T. D. Filippatos 1 • A. Liontos 1 • M. S. Elisaf 1 Received: 18 February 2016 / Accepted: 27 May 2016 Ó Asian Pacific Association for the Study of the Liver 2016 Abstract Hyponatremia (Na ? \ 135 mmol/l) is the most common electrolyte disorder. Cirrhosis represents a rather frequent cause of hyponatremia mainly due to systemic and splanchnic vasodilation resulting in decreased effective arterial blood volume, which leads to excessive non-os- motic secretion of antidiuretic hormone. However, hyponatremia of multifactorial origin may be seen in patients with liver diseases. The review focuses on the factors and pathogenetic mechanisms of decreased sodium levels other than the hemodynamic compromise of cir- rhosis in patients with liver diseases. The mechanisms and causal or contributing role of pseudohyponatremia, hyperglycemia, infections, drugs and toxins as well as of endocrine disorders, renal failure and cardiac disease in patients with liver disease are meticulously discussed. Hyponatremia of multifactorial origin is frequently observed in patients with liver diseases, and special efforts should be made to delineate the underlying causative and precipitating factors as well as the risk factors of the osmotic demyelination syndrome in order to properly manage this serious electrolyte disorder and avoid treat- ment pitfalls. Keywords Hyponatremia Á Liver disease Á Cirrhosis Á Infection Á Terlipressin Á Hepatitis Introduction Hyponatremia (Na ? \ 135 mmol/l) is the most common electrolyte disorder in hospitalized patients and in com- munity subjects [1–3]. Liver disease, especially cirrhosis, is a rather frequent cause of hyponatremia. In a prospective study of 204 hyponatremic patients admitted to an internal medicine clinic, cirrhosis was the cause of hyponatremia (defined as serum sodium concentration \ 130 mmol/l) in 20 (9.8 %) patients [4]. The incidence of hyponatremia is even higher in liver units. Indeed, in a prospective study of 997 patients with cirrhosis, 49.4 % of these patients exhibited serum sodium levels B135 mmol/l, and 21.6 % had serum sodium concentration B130 mmol/l [5]. The mechanisms of hyponatremia have been studied mainly in the context of cirrhosis, whereas other pathogenetic factors of this important electrolyte disorder in patients with liver disease have not been extensively investigated. In this review, we scrutinize the causes and/or superimposed factors as well as the clinical and pathophysiological aspects of hyponatremia in patients with liver disease, focusing on mechanisms other than the cirrhosis-induced hemodynamic compromise (Table 1; Fig. 1). Pathophysiology of hyponatremia Hyponatremia is attributed to either water retention or (less often) to loss of effective solute (sodium plus potassium) in excess of water. The capacity for water excretion is ade- quate in normal states; hence, retention of water resulting in decreased serum sodium levels is observed only in condi- tions that impair renal excretion of water. The exception to this rule is primary polydipsia in which the disproportionate water intake (10–15 l/per day) can overwhelm the normal & T. D. Filippatos filtheo@gmail.com 1 Department of Internal Medicine, School of Medicine, University of Ioannina, 451 10 Ioannina, Greece 123 Hepatol Int DOI 10.1007/s12072-016-9746-1