Antithrombin III metabolism in two patients with a nephrotic syndrome caused by minimal chain nephritis and primary amyloidosis.

The metabolism and urinary excretion of 125I antithrombin III (AT III) was investigated in 2 patients with a nephrotic syndrome caused by minimal chain nephritis and primary amyloidosis, and acquired deficiency of AT III. Increased AT III catabolism was observed in both patients, even after correction for urinary protein loss. Increased AT III catabolism was due to increased influx from the extra- to the intravascular compartment in 1 patient, and to an increased fractional catabolic rate in the other patient who developed later a pulmonary embolism. Analysis of urine samples revealed biologically inactive whole AT III molecules and biologically as well as antigenically inactive fragments, respectively, whereas daily plasma gel filtration showed intact radioactive AT III. These observations reject the hypothesis that AT III deficiency in nephrotic patients is only due to urinary loss of AT III.