Description

Continuous renal replacement therapy (CRRT) is a crucial intervention for managing acute kidney injury (AKI) in critically ill patients. Citrate anticoagulation has become a preferred method in CRRT due to its effect in longer filter longevity and less bleeding compared to unfractionated heparin1. However, its use in specific patient populations, such as those with liver failure or severe shock, necessitates careful evaluation.

Citrate acts as an anticoagulant by chelating calcium, an essential cofactor in the coagulation cascade, thus preventing clot formation within the extracorporeal circuit2. The citrate-calcium complex is then metabolized mainly in the liver, where citrate is converted into bicarbonate, and calcium is released back into the bloodstream. This mechanism provides dual benefits: effective anticoagulation and metabolic alkalization.

Patients with liver failure present unique challenges for citrate anticoagulation. Impaired liver function can lead to the accumulation of citrate, resulting in high anion gap metabolic acidosis and hypocalcemia3. These risks underscore the need for vigilant monitoring and potential adjustment of citrate dosing in this population. The aim of the present study is to explore whether the etiology of liver failure, which can range from alcoholic liver disease to drug-induced liver injury or shock liver, influences the incidence and severity of citrate-related complications.