The study included a prospective series of 444 patients who had been hospitalized for decompensated cirrhosis. Participants were divided into two: a study cohort (n=305) and a validation cohort (n=139). In the former cohort, factors associated with the outcome of 90-day mortality were first identified using bivariate analysis and refined using multivariate Cox regression models; such prediction models were confirmed in the validation cohort.
Over the 3-month follow-up period, 84 participants died in the study cohort. Compared to survivors, mortalities had significantly higher bilirubin, serum creatinine, and leukocyte counts, as well as model for end-stage liver disease sodium (MELD-Na) scores.
Of note, the urinary concentration of L-FABP was also significantly elevated among study cohort patients who died (median, 52 vs 27 µg/g creatinine; p=0.006).
Multivariate analysis found that the best model to predict 90-day mortality included urinary L-FABP levels combined with the MELD-Na score. The resulting C-statistic was 0.810. Both L-FABP and MELD-Na were significantly and independently predictive of both 90-day mortality and ACLF development.
The predictive value of the model was confirmed in the validation cohort, in which 36 patients (26 percent) died during follow-up. Multivariate analysis found that both urinary L-FABP and MELD-Na score were independently associated with 3-month mortality, with a resulting C-statistic of 0.819.
“The present study analysed urinary L-FABP levels in two independent groups of patients with decompensated cirrhosis and showed that higher urinary L-FABP levels correlated with increased mortality and risk of ACLF development,” the researchers said.
“Therefore, urinary L-FABP levels could be useful as a new tool to predict complications in patients with decompensated cirrhosis,” they added.