Sodium retention leading to the accumulation of fluid within the abdominal cavity in the form of ascites is the most common renal functional abnormality in advanced decompensated cirrhosis.1 The predominant mechanism underlying sodium retention in these patients is increased renal tubular sodium reabsorption secondary to exacerbated activity of the endogenous vasoactive systems and sodium retaining mechanisms. In fact, in cirrhosis and ascites, sodium retention takes place in the setting of a normal or moderately reduced glomerular filtration rate and increased activity of the renin-angiotensin-aldosterone system, one of the most powerful vasoconstrictor systems involved in body fluid homoeostasis.1 ,2

Whereas in decompensated cirrhosis the mechanism that initiates sodium retention and ascites formation is quite well established, in pre-ascitic cirrhosis it still remains a subject of interest and debate. Patients with compensated cirrhosis (patients without ascites on a normal sodium diet and without diuretics) usually do not exhibit sodium retention.1 Moreover, the activity …