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