Key result
Anticoagulation regimes in continuous renal replacement therapy are utilized to prevent circuit clotting by blocking contact activation, the coagulation cascade, or platelet activation.
This review discusses the mechanisms of coagulation in CRRT circuits and the rationale for various anticoagulation strategies in patients with acute renal failure.
Supports mechanism-informed anticoagulation selection in CRRT; extends mechanistic rationale while leaving optimal regimens open to randomized trials.
Although continuous renal replacement therapy (CRRT) provides greater cardiovascular and cerebrovascular stability compared to standard intermittent hemodialysis and/ or hemofiltration, to provide adequate solute removal, the CRRT circuit must function continuously. Patients with acute renal failure are usually prothrombotic, with activation of the contact coagulation cascade and reduction in the natural anticoagulants. Thus clotting within the extracorporeal circuit can be problematic. Coagulation requires activation of the coagulation protein enzymes, calcium, platelets, and contact with phospholipid cell surface or, in the case of the CRRT circuit, plastic tubing and the dialyzer membrane. This results in a platelet plug stabilized by cross-linking strands of fibrin. Anticoagulation regimes are either directed at trying to prevent contact activation of clotting factors and platelets or the administration of agents designed to prevent coagulation by blocking the coagulation cascade or platelet activation.
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Andrew Davenport (1998) conducted a review in Acute renal failure requiring continuous renal replacement therapy. Anticoagulation regimes was evaluated. Anticoagulation regimes in continuous renal replacement therapy are utilized to prevent circuit clotting by blocking contact activation, the coagulation cascade, or platelet activation.
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