Ascites formation in cirrhosis results from the interaction of "local" and "systemic" pathogenetic factors. Among local factors, post-sinusoidal portal hypertension plays the most important role, while the main systemic event is renal sodium retention. The latter precedes ascites formation and leads to plasma volume expansion. Many factors are responsible for renal sodium retention, but secondary hyperaldosteronism and reduced renal perfusion prevail. The events promoting the onset of sodium retention are far from being clarified. However, there is evidence that the main afferent mechanism is represented by the "effective" hypovolemia secondary to splanchnic venous vasodilation, due to portal hypertension, and reduced peripheral vascular resistance, which becomes evident in the advanced stage of the disease. Systemic hemodynamic abnormalities are responsible for the progressive reduction of renal perfusion, which ends in the hepatorenal syndrome. The appearance of ascites is a crucial event in the natural history of cirrhosis and has a negative prognostic meaning. In fact, ascites appears when pathogenetic factors, such as liver function abnormalities, portal and systemic hemodynamics, and renal function, have reached a critical threshold severity. Second, ascites itself induces additional complications, closely linked to its presence, such as spontaneous bacterial peritonitis, restrictive respiratory failure, or rupture of abdominal hernias. Finally, ascites implies pharmacological or invasive treatment which can lead to further morbidity or even to death.