[1] The SAAG may be a better discriminant than the older method of classifying ascites fluid as a transudate versus exudate.
This balance is disturbed in certain diseases (such as the Budd–Chiari syndrome, heart failure, or liver cirrhosis) that increase the hydrostatic pressure in the circulatory system.
The SAAG subsequently increases because there is more free fluid leaving the circulation, concentrating the serum albumin.
A rare cause of ascites, with elevated SAAG, and without change in hydrostatic/osmotic pressure is urinary bladder rupture with leakage of urine into the peritoneal space.
[2] This is due to increased hydrostatic pressure within the blood vessels of the hepatic portal system, which in turn forces water into the peritoneal cavity but leaves proteins such as albumin within the vasculature.