Minimal-change glomerulonephritis associated with circulating anticoagulant to factor XII.
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The fortuitous detection of an increased activated cephalin clotting time is often dependent on defects of the blood-clotting factors synthesized by the liver, haemophilia or von Willebrand's disease, circulating anticoagulants or specific deficiencies of various factors necessary for blood-clotting mechanisms. Much more rarely, it may be due to an isolated Hageman factor defect. This deficiency does not lead to an increased bleeding tendency and surgery has proved surprisingly uneventful. On the other hand, thromboembolic events may appear. Being and inherited disease with autosomal recessive transmission, the discovery of Hageman factor deficiency must lead to a complete family investigation.
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