Regional citrate anticoagulation for renal replacement therapy

Abstract

Citrate causes anticoagulation by chelation of ionized calcium in the extracorporeal circuit. Systemic anticoagulation does not occur if the patient’s serum-ionized calcium is restored. Citrate anticoagulation also reduces the activation of leukocytes and platelets inside the circuit. Citrate molecules injected into the circuit generate Calcium-citrate complexes, partly eliminated by the membrane. Calcium-citrate complexes remaining in the circuit after membrane exchanges are injected to the patient and metabolized by the tricarboxylic acid cycle of the cells, mainly in the liver, releasing bicarbonate and ionized calcium. An intravenous supply of calcium is therefore necessary to compensate for the eliminated calcium amounts by the membrane. In continuous renal replacement therapy, regional citrate anticoagulation is associated with a longer lifespan of the circuits and a lower risk of bleeding. In intermittent hemodialysis, citrate anticoagulation is less used. There is no direct toxicity from citrate. The side effects of citrate anticoagulation are essentially a risk of hypo or hypercalcemia for the patient in case of inappropriate calcium supply and acid-base disturbances if the genesis of bicarbonate by citrate metabolization is not taken into account in the solutes used renal replacement.