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Mechanisms of the development of acquired antithrombin III deficiency in the experimental nephrotic syndromes.

In the experiments on white rats was studied the role of excessive thrombinogenesis in the development of acquired antithrombin III deficiency in the experimental nephrotic syndrome. It was determined that excess thrombin generation induced the marked acceleration of 125I-antithrombin III clearance from blood stream in consequence formation of thrombin antithrombin III complexes with the following limited proteolysis of the inhibitor by enzyme. These results give evidence that apart from proteinuria the excess thrombin generation accompanied by nephrotic syndrome play a part in the development of acquired deficiency of antithrombin III in this experimental pathology.