Table 2 Advantages and disadvantages of heparin or citrate anticoagulation during continuous renal replacement therapy

   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