Increased kidney absorption of salt and solute-free water resulting in volume overload is frequently observed in cirrhosis, especially with progression of the disease. Although diuretic therapy is able to control volume overload in the early stages of cirrhosis, it fails in a significant proportion of patients in late stages, giving rise to a situation termed "diuretic resistant ascites." This situation represents a state of functional renal failure called hepatorenal syndrome, which is further classified into 2 subgroups based on the severity of renal failure. Although many proposed stimuli have been suggested in the past to explain the pathophysiology behind this maladaptive renal response to advanced liver disease, the peripheral arterial vasodilation hypothesis has been the one that gained wide popularity. Nevertheless, many pieces of evidence, both old and new, are not completely compatible with this hypothesis, suggesting that vascular bed vasodilation in cirrhosis could be a consequence of blood shunting from the portal to the systemic circulations rather than an etiology for volume overload. At the same time, an accumulating body of evidence has been pointing toward a direct interaction between the liver and the kidneys that may have an etiologic role for volume overload. Therefore, looking for a new hypothesis for volume overload in cirrhotics is of paramount importance to explain the pathophysiology behind this neat observation and to understand the available options to deal with this morbid complication of cirrhosis.