Abstract

Abstract Background and Aims Continuous renal replacement therapy (CRRT) is pivotal for managing acute kidney injury (AKI) unstable patients. However, questions persist regarding prescription and the role of anticoagulation. This study aims to examine CRRT practices, focus on citrate-based anticoagulation and clarify contraindications. Method This study comprises a retrospective analysis of a patient cohort requiring CRRT and admitted to the Postoperative Intensive Care Unit and Burn Unit. Inclusion criteria involved the need for CRRT and adult age, with exclusion criteria based on treatment duration (<48 hours), reducing the initial cohort from 256 to 176 patients. Clinical variables, including gender, age, underlying pathology, CRRT modality, and anticoagulation type, were characterized. Subsequently, the association between anticoagulation type and clot formation within 48 hours and in-hospital mortality was investigated. Furthermore, an analysis of citrate-based CRRT was conducted, evaluating laboratory values (Table 1) at the beginning and 48 hours using the Wilcoxon test, and their correlation with clot development and mortality. Additionally, we used a logistic regression model to explore the relationship between AST, ALT, and lactate values with citrate accumulation. Finally, a survival analysis was conducted. Results The sample consisted of 66.5% males and 33.5% females, with an average age of 59.48 years. Reasons for admission are depicted in Fig. 1. CRRT modalities were 20.5% HDVVC, 76.1% HDFVVC, and 3.4% HFVVC. Anticoagulation included 35.2% none, 28.4% heparin, 33.5% citrate, and 2.8% alprostadil. Filter clotting occurred in 29.1% withing 48 hours. Heparin was associated with a 5.4-fold increased risk of clotting compared to citrate. Mortality was 63.3%, with no anticoagulation type showing a significant association. Parameters at CRRT initiation and 48 hours for citrate-based CRRT patients and Wilcoxon test results are presented in Table 1. Only 5.1% had filter clotting <48 hours, and no baseline parameters were significantly associated with an increased clotting risk. There was one case of citrate intoxication due to a programming error, which was not included. 76.81% had CaT/CaI <2.1, and 7.25% had CaT/CaI >2.1, requiring technique adjustments. Aminotransferases and lactate values, often considered as contraindications for citrate, were analyzed: The average AST and ALT values were 188.53 IU/l and 108.08 IU/l, respectively. When AST levels exceeded 5 times the normal range and ALT levels exceeded 3 times the normal range, a statistically significant association with CaT/CaI >2.1 at the 48-hour mark of CRRT utilization was observed (p < 0.001 for both).The average lactic acid value was 1.74 mg/dl. Having a lactic acid level >4 was associated (p < 0.05) with a higher risk of developing CaT/CaI >2.1. 54.2% of the sample died. No baseline parameters were significantly associated with it. At 48 hours, higher bicarbonate levels and metabolic alkalosis were associated with increased mortality (p < 0.05). The median survival time was 11 days (±4.38). Conclusion This study supports the use of citrate-based anticoagulation in CRRT, as no cases of citrate intoxication (CaT/CaI >2.5) were found. Nonetheless, a significantly elevated AST (>5 times normal), ALT (>3 times normal), and lactate (>4 mg/dl), were associated with a higher risk of citrate accumulation (CaT/CaI >2.1). Customized approaches and preventive measures to mitigate the development of metabolic alkalosis are essential for optimizing patient outcomes.

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