Renal sodium retention in pre-ascitic cirrhosis: the more we know about the puzzle, the more it becomes intricate.

Ascites develops in 5–10% of patients with compensated cirrhosis per year and carries an ominous prognosis [1] . The appropriate management and possible prevention of this complication obvi- ously depends on an in-depth knowledge of ascites pathophysiol- ogy, which remains somewhat elusive despite many studies that have addressed the topic over decades. There is no doubt that post-sinusoidal portal hypertension is the main ‘‘local” pathoge- netic factor, and renal sodium retention is the main ‘‘systemic” event leading to a positive fluid balance and, ultimately, ascites formation. However, uncertainties surround both the efferent (that is the factors/systems promoting renal sodium retention) and afferent (that is the factors that activate efferent mecha- nisms) factors associated with renal sodium handling abnormal- ities [2] . Sodium balance has been demonstrated to become positive before ascites formation both in animal models of cirrho- sis and humans [3–6] . Study of the early mechanisms leading to ascites would help unveil its pathophysiology in a stage of the disease where further complications involving systemic hemody- namics and renal function may act as confounding factors. In this issue of the Journal of Hepatology, Sansoè and co-workers pres- ent a fine study on an efferent mechanism potentially leading to renal sodium retention in pre-ascitic cirrhosis