Efficacy and Safety of Citrate Anticoagulation in CRRT for Patients With Liver Failure/DysfuncTION, the CAUTION Trial! A Retrospective Study on Etiology of Liver Failure and Their Complications

Last updated: April 2, 2025
Sponsor: University Hospital, Antwerp
Overall Status: Active - Recruiting

Phase

N/A

Condition

Liver Failure

Kidney Disease

Liver Disease

Treatment

N/A

Clinical Study ID

NCT06908746
Project ID 6806
Edge 003873
  • Ages > 18
  • All Genders

Study Summary

Study design A retrospective cohort study will be conducted to compare the efficacy and safety of citrate anticoagulation in CRRT among patients with liver failure/dysfunction and severe shock.

Objectives

  1. Primary Objective: To determine if the etiology of liver failure impacts the incidence of citrate-related complications in patients undergoing CRRT.

  2. Secondary Objectives: To compare the efficacy of citrate anticoagulation in terms of renal recovery, filter lifespan, and patient survival between those with liver failure/dysfunction and severe shock.

Eligibility Criteria

Inclusion

Inclusion Criteria:

  • Critically ill patients diagnosed with AKI requiring CRRT. Caution Protocol V1.0 24-07-2024

  • Documented liver failure or significant liver dysfunction (e.g., elevated liverenzymes, bilirubin levels, or clinical diagnosis of liver failure) and clincaldiagnosis of shock (NE of 0.25 μg/kg/min and or association of second vasopressor).

  • Age ≥ 18 years.

Exclusion

Exclusion Criteria:

  • NA

Study Design

Total Participants: 100
Study Start date:
September 30, 2024
Estimated Completion Date:
December 31, 2025

Study 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.

Connect with a study center

  • Antwerp University Hospital

    Edegem, Antwerp 2650
    Belgium

    Active - Recruiting

Not the study for you?

Let us help you find the best match. Sign up as a volunteer and receive email notifications when clinical trials are posted in the medical category of interest to you.