Ascites kinetics in cirrhosis: effects of rapid volume expansion and diuretic administration.

I examined whether the rate of ascites formation in cirrhosis is increased by volume expansion and whether this rate is related to the intensity of renal sodium retention, and I examined the mechanisms by which ascites is mobilized during diuresis. The plasma-ascites filtration rate (PFR) of intravenously injected iodine 125-labeled albumin (the rate of ascites formation by the liver) after volume expansion with normal saline solution in seven patients was similar to that observed in 14 patients who had not received infusions (0.010 +/- 0.003 vs. 0.013 +/- 0.006 L/hr/m2) and was unrelated to natriuresis both before and after intravenous administration of 80 mg furosemide the previous day (r = 0.04 and -0.36). Diuresis of seven patients who had not received infusions reduced PFR (from 0.679 +/- 0.267 to 0.411 +/- 0.198 L/day, P less than 0.05) and total ascites formation rate (from 3.029 +/- 1.620 to 1.465 +/- 1.053 L/day, P less than 0.02) but not plasma volume (from 3.464 +/- 0.646 to 3.391 +/- 0.775 L). Increases occurred in ascites albumin concentration (from 7 +/- 4 to 9 +/- 4 gm/L, P less than 0.05) and in the ascites/serum albumin ratio (from 0.26 +/- 0.12 to 0.35 +/- 0.13, P less than 0.05) but not in the serum-ascites albumin gradient (portal pressure). Fractional changes in ascites volume and albumin concentration were unrelated (r = 0.20). The calculated rate of ascites reabsorption decreased in five patients during diuresis, indicating that ascites was mobilized by decreased formation. Ascites reabsorption increased in two patients.(ABSTRACT TRUNCATED AT 250 WORDS)