000			03277nam a22003617a 4500
003			OSt
005			20240305193725.0
008			221110b |||||||| |||| 00| 0 eng d
028			_b Phone: +255 28 298 3384
028			_b Fax: +255 28 298 3386
028			_b Email: vc@bugando.ac.tz
028			_bWebsite: www.bugando.ac.tz
040			_cDLC
041			_aEnglish
100			_aQun-Qun Jiang _945233
222			_a Decompensated cirrhosis, Acute-on-chronic liver failure, Acute kidney injury, Biomarker, Etiology, Treatment, Prognosis
245			_aAcute kidney injury in acute-on-chronic liver failure is different from in decompensated cirrhosis
260			_aMwanza: _b Baishideng Publishing Group Inc & _b Tanzania Catholic University of Health and Allied Sciences [CUHAS – Bugando] _c2018/6/6
300			_aPages 2300
490			_vWorld journal of gastroenterology Volume 24 Issue 21
520			_aAbstract AIM: To evaluate the differences in acute kidney injury (AKI) between acute-on-chronic liver failure (ACLF) and decompensated cirrhosis (DC) patients. METHODS: During the period from December 2015 to July 2017, 280 patients with hepatitis B virus (HBV)-related ACLF (HBV-ACLF) and 132 patients with HBV-related DC (HBV-DC) who were admitted to our center were recruited consecutively into an observational study. Urine specimens were collected from all subjects and the levels of five urinary tubular injury biomarkers were detected,including neutrophil gelatinase-associated lipocalin (NGAL), interleukin-18 (IL-18), liver-type fatty acid binding protein (L-FABP), cystatin C (CysC), and kidney injury molecule-1 (KIM-1). Simultaneously, the patient demographics, occurrence and progression of AKI, and response to terlipressin therapy were recorded. All patients were followed up for 3 mo or until death after enrollment. RESULTS: AKI occurred in 71 and 28 of HBV-ACLF and HBV-DC patients, respectively (25.4% vs 21.2%, P = 0.358). Among all patients, the levels of four urinary biomarkers (NGAL, CysC, L-FABP, IL-18) were significantly elevated in patients with HBV-ACLF and AKI (ACLF-AKI), compared with that in patients with HBV-DC and AKI (DC-AKI) or those 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 of ACLF-AKI patients was significantly lower than that of patients with DC-AKI (32.6% vs 57.9%, P = 0.018). Furthermore, patients with ACLF-AKI had the lowest 90 d survival rates among all groups (P < 0.001). CONCLUSION: AKI in ACLF patients is more likely associated with structural kidney injury, and is more progressive, with a poorer response to terlipressin treatment and a worse prognosis than that in DC patients.
700			_a Mei-Fang Han _945234
700			_a Ke Ma _945235
700			_a Guang Chen _945236
700			_a Xiao-Yang Wan _945237
700			_aSemvua Bukheti Kilonzo _922895
700			_a Wen-Yu Wu _945238
700			_aYong-Li Wang _945239
700			_aJie You _945240
700			_aQin Ning _945241
856			_u10.3748/wjg.v24.i21.2300
942			_2ddc _cVM
999			_c19366 _d19366