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Recurrent Intravascular Coagulation with Renal Cortical Necrosis and Recovery

P. W. STRAUB, M.D.; A. VON FELTEN, M.D.; and P. G. FRICK, M.D., PH.D.
Ann Intern Med. 1966;64(3):643-654. doi:10.7326/0003-4819-64-3-643
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This excerpt has been provided in the absence of an abstract.

Acquired hypofibrinogenemia is due either to a decreased rate of fibrinogen production in the liver or to an increased rate of disappearance from the circulating blood. The latter mechanism can be the result of intravascular coagulation or accelerated fibrinolysis. Whereas the development of thrombolytic therapy has introduced a unique tool for investigation of pure fibrinolytic states, it is not possible to induce intravascular coagulation experimentally in man. Progress in the basic understanding of this condition is therefore dependent on careful investigation of human cases of acquired hypofibrinogenemia.

The case reported below is an example of acquired acute hypofibrinogenemia in a


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