Medical treatment of ascites is aimed at reverting sodium retention, t
hat is, at creating a negative sodium balance to relieve ascites. Bed
rest and low-sodium diet induce the disappearance of ascites in about
10% of patients. Loop diuretics and aldosterone antagonists must be ad
ministered to the patients not responding to the previous regimen. Ava
ilable evidence indicates that aldosterone antagonists are the first-c
hoice drugs, as these substances are more effective than furosemide. N
evertheless, loop diuretics potentiate the effects of aldosterone anta
gonists. The reduced efficacy of furosemide in these patients, when co
mpared with that of spironolactone, may be related to an impairment of
both pharmacodynamics and pharmacokinetics. In fact, most sodium not
reabsorbed in Henle's loop, due to the action of furosemide, is subseq
uently taken up in the distal nephron because of hyperaldosteronism. A
further mechanism of resistance may be related to an impaired excreti
on of furosemide into the tubular lumen. The use of diuretics in the t
reatment of ascites is associated with several side effects, including
prerenal azotemia, hepatic encephalopathy, and electrolyte and acid-b
ase disorders. A stepped-care approach, together with careful monitori
ng of patients, is the best way to reduce the incidence of these compl
ications. Ethacrynic acid has been shown to be highly effective in the
treatment of ascites, even in patients refractory to other diuretics,
but its use is associated with a high incidence of hypokalemia and hy
pochloremic alkalosis. Bumetanide and piretanide are comparable to fur
osemide, in terms of both efficacy and side effects. Recent data sugge
st that torasemide, administered in equipotent doses to furosemide, ex
erts a higher natriuretic and diuretic effect, together with a similar
kaliuretic effect.