Table 2.

Advantages and disadvantages of heparin or citrate anticoagulation during continuous renal replacement therapy

	Heparins	Citrate
Clinical
Anticoagulation	Regional and systemic	Regional, not systemic
Risk of bleeding	Higher	Not increased
Circuit life	Similar or shorter	Similar or longer
Metabolic control	Good	Good if well performed
Metabolic derangements		Greater risk if not well controlled
Understanding	Easy	Difficult
Life-threatening complications	Massive bleeding
	Heparin-induced thrombocytopenia (UFH >LMWH)	Cardiac arrest due to unintended rapid infusion
Clinical outcome		Possibly better patient and kidney survival
Biochemical
Anticoagulation	Critically ill patients exhibit heparin resistance due to:
	• Low antithrombin (high consumption and degradation)
	• Acute phase proteins and apoptotic/necrotic cells bind heparin (UFH >LMWH)
Proinflammatory effects	Inhibit the anti-inflammatory properties of antithrombin (UFH >LMWH)
	Trigger antithrombin degradation by elastase
	Release myeloperoxidase, elastase, platelet factor 4, superoxide dismutase into the circulation (UFH, LMWH)
	Increase in lipopolysaccharide-induced, LPB-dependent IL-8 and IL-1β secretion from monocytes (LMWH, UFH)
Anti-inflammatory effects	Inhibit thrombin generation (UFH, LMWH)	Its use prevents the release of granular products from neutrophils and platelets
	Block P-selectin and L selectin-mediated cell adhesion (UFH, LMWH)
	Decrease cytokine generation in vitro, not in vivo
Phagocytosis	Bind to apoptotic and necrotic cells and may delay phagocytic clearance (UFH >LMWH)
Bio-energetic properties		Provides energy without needing insulin for entrance into the cell
		May protect against mitochondrial dysfunction

UFH, unfractionated heparin; LMWH, low molecular weight heparin; LBP, lipopolysaccharide-binding protein.