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About half of all patients with compensated cirrhosis will develop ascites within 5 years.1 Hence, the management of ascites is a major task for physicians caring for patients with advanced cirrhosis. Ascites results from the interplay of local and systemic pathogenetic factors, mainly portal hypertension and renal retention of sodium and water. Sodium and water retention is induced by a reduction in effective volaemia that results from peripheral arterial vasodilation,2 leading to the activation of sodium retaining systems, namely the renin–angiotensin–aldosterone axis, and ultimately hampering renal perfusion. Renal sodium retention aims at expanding extracellular fluid volume, including total plasma volume, which can be seen as a crucial compensatory factor against effective hypovolaemia.
Paracentesis is the first-line treatment for massive or refractory ascites.3 4 However, diuretics remain the mainstay of medical therapy for moderate ascites,3 4 and are also required to prevent or delay further paracentesis in patients with massive peritoneal effusion.5 As renal perfusion and glomerular filtration rate (GFR) are fairly well preserved in the early stages of ascitic decompensation, secondary hyperaldosteronism is the principal pathogenetic factor, and sodium retention mainly occurs at the distal nephron. In more advanced stages, once GFR has declined, proximal sodium reabsorption progressively increases and may become prevalent. A rational choice of diuretics …
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