Ascites is the most common decompensating event in cirrhosis [1]. Its pathophysiology involves splanchnic arterial vasodilation and reduced effective arterial blood volume, which activate potent vasoconstricting and sodium retaining mechanisms, such as the renin-angiotensin-aldosterone system [2]. However, sodium retention occurs mainly at the proximal nephron sites whereas loop diuretics and mineralocorticoid receptor antagonists act at distal segments. Eventually, up to 10 % of patients with cirrhosis will develop refractory ascites (RA) due to avid renal sodium and fluid retention which portends poor prognosis.
