• 1 January 1981
    • journal article
    • research article
    • Vol. 76  (5) , 423-431
Abstract
The mechanism of increase in the protein concentration of ascitic fluid during diuresis was investigated in 27 patients with chronic liver disease. The albumin concentration increased in ascites from 0.58 .+-. 0.49 gm% in the initial paracentesis to 1.48 .+-. 0.69 gm% in the final paracentesis (P < 0.001) as the serum albumin concentration increased from 2.40 .+-. 0.44 gm%-2.94 .+-. 0.56 gm% (P < 0.001). The serum to ascites albumin concentration gradient decreased significantly from 1.82 .+-. 0.39 gm%-1.46 .+-. 0.45 gm% (P < 0.001). Despite this decrease, the serum to ascites albumin concentration gradient was relatively constant (decrease of 0.36 gm% or 20% of initial value) compared to the absolute or percentage change in ascites total protein concentration (increase of 1.48 gm% or 107% of initial value). In 4 patients studied prospectively, the plasma volume did not change (3.53 .+-. 0.80 1-3.73 .+-. 0.59 l) during diuresis, despite increase in total intravascular albumin (85.7 .+-. 25.6 gm-99.9 .+-. 22.3 gm); P < 0.05) and decrease in total albumin in combined intravascular and peritoneal compartments (156.0 .+-. 30.1 gm-143.4 .+-. 35.3 gm; P < 0.05). Since neither concentration without decrease in plasma volume or synthesis of protein without increase in total compartental protein appear to be the major mechanism of serum protein concentration increase, the increase in serum protein concentration was attributed to redistribution of protein from ascites to the intravascular compartment. The increase in ascitic fluid protein concentration during diuresis can be attributed to an increase in serum protein concentration in the presence of the relatively stable serum to ascites albumin concentration gradient.