Editorial Ancrod in

In 1963 incoagulable blood was observed in victims bitten by the Malayan pit viper (Agkistrodon rhodostomd) [1], and ancrod, the factor responsible, was subsequently isolated. Ancrod is a highly specific protease which has a thrombin-like effect on fibrinogen, but results in the formation of an unstable fibrin clot which is readily dispersed and rapidly lysed. Ancrod administration thus leads to rapid depletion of plasma fibrinogen. Controlled defibrinogenation can be maintained for several weeks by daily infusions of ancrod, with dose adjustments according to response. If overdose occurs the effect car) be reversed rapidly by infusion of fibrinogen and antivenene. Extensive experience in deep vein thrombosis and other thrombotic disease suggests that the risk of haemorrhagic complications may be less than with heparin, and that other side-effects are very rare [2]. What has this to do with glomerulonephritis? In a variety of severe acute renal diseases, including proliferative glomerulonephritides, lupus nephritis, and the thrombotic micro-angiopathies, fibrin can be shown to be present in capillary loop thrombi, or in Bowman's space where it is believed to stimulate crescent formation. The associated clinical picture is often one of rapidly progressive glomerulonephritis, where progressive irreversible glomeru