Published online Jun 7, 2018. doi: 10.3748/wjg.v24.i21.2300
Peer-review started: March 28, 2018
First decision: April 19, 2018
Revised: April 28, 2018
Accepted: May 6, 2018
Article in press: May 6, 2018
Published online: June 7, 2018
Acute kidney injury (AKI) is a common and serious complication of acute-on-chronic liver failure (ACLF) and decompensated cirrhosis (DC). Previous studies have been clearly established that the acute-on-chronic liver failure and decompensated liver cirrhosis are two different diseases.However, the differences in acute kidney injury among patients with these two diseases are rarely studied and whether AKI should be managed in the same way in patients with these two diseases is still uncertain.
Clinically, the treatment of patients with different types of renal impairment is significantly different. A clear clarification on the differences in AKI between ACLF and DC patients will promote timely and more appropriate management of the patients.
This study was conducted to clarify the differences in AKI between hepatitis B virus (HBV)-ACLF and HBV-DC patients, including the differences in the etiology of AKI, natural course, patient’s response to terlipressin and prognosis.
This study is a prospective observational study, patients with HBV-ACLF and HBV-DC who were admitted to our hospital between 2015.12 and 2017.7 were consecutively recruited. Urine specimens of all patients were collected at the time of admission and when AKI was diagnosed, and the levels of five tubular injury biomarkers in urine were detected. Simultaneously, the demographic data, natural course of AKI, patient’s response to terlipressin treatment and patient outcomes were recorded.
Patients with ACLF-AKI have significantly higher urinary biomarker levels than those with DC-AKI or without AKI. There was a higher proportion of patients with AKI progression in ACLF-AKI patients than in DC-AKI patients (49.3% vs 17.9%, P = 0.013). Forty-three patients with ACLF-AKI and 19 patients with DC-AKI were treated with terlipressin, the response rate to terlipressin was significantly lower in patients with ACLF-AKI than in patients with DC-AKI (32.6% vs 57.9%, P = 0.018). In addition, patients in the ACLF-AKI group had the lowest survival rate at 90 d among all groups (P < 0.001).
Our study demonstrated that AKI in patients with HBV-ACLF is distinct different from in HBV-DC patients.In HBV-ACLF patients, AKI is more likely to be caused by structural damages and tends to be more progressive, with a poorer response to terlipressin and a worse prognosis than in HBV-DC patients.
Our results suggest that AKI occurring in patients with HBV-ACLF or HBV-DC should be managed in different ways. Large-scale multi-center studies are required to validate these findings, and the differences in AKI between patients with ACLF and DC caused by other etiologies still need to be further studied.