The role of urinary biomarkers in the diagnosis of acute kidney injury in patients with liver cirrhosis

Abstract

AKI is common in patients with liver cirrhosis (LC) affecting (30 to 50%). Our study aimed to evaluate the role of urinary biomarkers as predictors of AKI, its etiology and mortality. We performed a prospective cohort study of patients with LC during 1 year. Urine samples for biomarkers dosage were collected within 48 h of hospital admission. Diagnosis of AKI was performed according to KDIGO 2012 criteria. The results were presented using Chi-square, T test, AUC-ROC and logistic regression (p < 0.05). We included 100 patients, 58.5 ± 16.1 years, main etiologies of LC were alcohol and and metabolic disfunction associated with steatohepatitis. Infection was the main cause of LC decompensation. AKI occurred in 53% of patients and mortality was 20%. CHILD C, infectious as cause of decompensation, baseline creatinine, need for mechanical ventilation and noradrenaline use and urinary were associated with AKI. We found no association between AKI and KIM-1 and IL-18. The main etiologies of AKI were transient ischeamia (49%), renal (43.4%), and hepatorenal syndrome (HRS) (7.5%). There was difference between the groups in hematuria, proteinuria, FENa, FEUr and uNGAL which were higher in renal AKI when compared to transient ischaemia and HSR. FENa and FEUr were excellent predictors of AKI etiology (AUC-ROC > 0.80, sensitivity and specificity > 0.80), while only uNGAL was good predictor of AKI etiology (AUC-ROC, sensitivity and specificity > 0.70). Regarding death, CHILD C, baseline creatinine, KDIGO 3, septic AKI, need for mechanical ventilation and IL-18 were identified as associated variables. Only NGAL was predictor of AKI and its etiology, anticipating AKI diagnosis in 2.5 ± 1.1 days, while IL-18 was predictor of death. We highlight the importance of lower-cost biochemical tests as FENa and FEUr and clinical information as CHILD and cause of LC descompensation which were relevant in predicting AKI, its etiology and death.

Keywords: Acute kidney injury; Biomarkers; Liver cirrhosis.

Fig. 1

Patients included in the study (flowchart).

Fig. 2

ROC analysis of uNGAL in pacientes with liver cirrhosis with AKI vs. non-AKI.

Fig. 3

(A) ROC analysis of uNGAL in pacientes with liver cirrhosis with AKI renal vs. transient ischaemia or HRS. (B) ROC analysis of FENa in patients with liver cirrhosis with AKI renal vs. transient ischaemia or HRS. (C) ROC analysis of FEUr in patients with liver cirrhosis with AKI renal vs. transient ischemia or HRS.

Fig. 4

ROC analysis of IL-18 in survival vs. non-survival patients with liver cirrhosis.

Fig. 5

(A) Forest plot for risk factors for AKI. (B) Forest plot for risk factors for death.