'Diuretic-resistant' ascites. Observations on pathogenesis.

Hepatic sinusoidal hydrostatic-oncotic balance was measured in 25 patients with alcoholic liver disease and varying severity of sodium retention. Eight patients had diuretic-responsive ascites and 17 patients had diuretic-resistant ascites. Net "transfer pressure," the force theoretically favoring fluid transudation across the hepatic sinusoids, was similar in the diuretic-responsive and diuretic-resistant groups and was unrelated to the fractional excretion of sodium after intravenous administration of furosemide. Fractional sodium excretion was significantly less in resistant than in responsive patients, but kaliuresis after furosemide was similar. Baseline creatinine clearance was similar in the two groups, but maximal oral diuretic therapy caused a significantly steeper rise in serum creatinine concentration in resistant than in responsive patients, despite less weight loss. More marked hepatic sinusoidal hydrostatic-oncotic imbalance was not present in patients with diuretic-resistant ascites. Similar kaliuretic response despite reduced natriuretic response to furosemide suggested that the proximal tubule is the site of enhanced sodium resorption in these patients. Renal insufficiency developing during long-term diuretic treatment is an important factor limiting natriuresis in patients with diuretic-resistant ascites.