Key result
Anticoagulation regimens for continuous renal replacement therapy in acute renal failure aim to prevent extracorporeal circuit clotting by blocking the coagulation cascade or platelet activation.
This review outlines the mechanisms of circuit clotting and the rationale for various anticoagulation strategies in patients with acute renal failure undergoing continuous renal replacement therapy.
Clarifies anticoagulation rationale in CRRT; leaves open optimal regimen selection pending higher-level evidence.
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. Anticoagulation was evaluated. Anticoagulation regimens for continuous renal replacement therapy in acute renal failure aim to prevent extracorporeal circuit clotting by blocking the coagulation cascade or platelet activation.
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