Lupus nephritis with XXXX and abnormal fibrinolysis: effect of ancrod.

@entity1 @entity8 @entity1252 @entity1351 @entity74 @entity715 @entity631
Recent evidence demonstrates that coagulation plays a role in mediating @entity8 in @entity1 with @entity1252 and @entity631 . Because of its beneficial effect in experimental @entity631 , we treated @entity1 with @entity1252 and @entity631 with ancrod, a drug known to lower fibrinogen levels and thought to activate fibrinolysis. Our @entity1 had unusually severe @entity8 ; renal function was deteriorating in many. Before ancrod, vascular plasminogen activator levels were low, and levels of an inhibitor of plasminogen activation were elevated. Some @entity1 had elevated @entity1351 inhibitor levels. Results were considered in two groups. In 13 @entity1 characterized as fibrinolysis responders, the low vascular plasminogen activator and increased plasminogen activation inhibitor levels normalized. After ancrod, striking resolution of microvascular @entity715 occurred, which was associated with some improvement in renal function and blood pressure control. In five @entity1 characterized as fibrinolysis nonresponders and who also had an elevated @entity1351 inhibitor (alpha 2-antiplasmin) level, normalization of fibrinolysis did not occur. There was little change in microvascular @entity715 , renal function, or blood pressure control in the fibrinolysis nonresponders. These preliminary observations demonstrate a @entity74 in @entity1 with @entity1252 with microvascular thrombi in the kidney. Ancrod therapy reverses this disorder rapidly in @entity1 with a normal level of @entity1351 inhibitor and may lead to repair of @entity8 .
