Ascites is the most common complication of cirrhosis, and 60% of patients with compensated cirrhosis develop ascites within 10 years during the course of their disease. Ascites only occurs when portal hypertension has developed [2] and is primarily related to an inability to excrete an adequate amount of sodium into urine, leading to a positive sodium balance. A large body of evidence suggests that renal sodium retention in patients with cirrhosis is secondary to arterial splanchnic vasodilation. This causes a decrease in effective arterial blood volume with activation of arterial and cardiopulmonary volume receptors, and homeostatic activation of vasoconstrictor and sodium-retaining systems (i.e., the sympathetic nervous system and the renin–angiotensin–aldosterone system). Renal sodium retention leads to expansion of the extracellular fluid volume and formation of ascites and edema. The development of ascites is associated with a poor prognosis and impaired quality of life in patients with cirrhosis. Thus, patients with ascites should generally be considered for referral for liver transplantation. There is a clear rationale for the management of ascites in patients with cirrhosis, as a successful treatment may improve the outcome and symptoms.