Xiangbo Xu1, Bang Liu2, Su Lin3, Bimin Li4, Yunhai Wu5, Yiling Li6, Qiang Zhu7, Yida Yang8, Shanhong Tang9, Fanping Meng10, Yu Chen11, Shanshan Yuan12, Lichun Shao13, Mauro Bernardi14, Eric M Yoshida15, Xingshun Qi16. 1. Department of Gastroenterology, General Hospital of Northern Theater Command (Formerly Called General Hospital of Shenyang Military Area), Shenyang, China. 2. Department of Hepatobiliary Disease, Fuzong Clinical Medical College of Fujian Medical University & 900 Hospital of the Joint Logistics Team, Fuzhou, China. 3. Liver Research Center, The First Affiliated Hospital of Fujian Medical University, Fuzhou, China. 4. Department of Gastroenterology, The First Affiliated Hospital of Nanchang University, Nanchang, China. 5. Department of Critical Care Medicine, The Sixth People's Hospital of Shenyang, Shenyang, China. 6. Department of Gastroenterology, The First Affiliated Hospital of China Medical University, Shenyang, China. 7. Department of Gastroenterology, Shandong Provincial Hospital Affiliated to Shandong University, Jinan, China. 8. State Key Laboratory for Diagnosis and Treatment of Infectious Diseases, Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, College of Medicine, The First Affiliated Hospital, Zhejiang University, Hangzhou, China. 9. Department of Digestive diseases, General Hospital of Western Theater Command, Chengdu, China. 10. Department of Biological Therapy, The Fifth Medical Center of PLA General Hospital, Beijing, China. 11. Difficult and Complicated Liver Diseases and Artificial Liver Center, Beijing YouAn Hospital, Capital Medical University, Beijing, China. 12. Department of Gastroenterology, Xi'an Central Hospital, Xi'an, China. 13. Department of Gastroenterology, Air Force Hospital of Northern Theater Command, Shenyang, China. 14. Department of Medical and Surgical Sciences, University of Bologna, Bologna, Italy. 15. Division of Gastroenterology, Vancouver General Hospital, Vancouver, BC, Canada. 16. Department of Gastroenterology, General Hospital of Northern Theater Command (Formerly Called General Hospital of Shenyang Military Area), Shenyang, China. xingshunqi@126.com.
Abstract
BACKGROUND: Acute gastrointestinal bleeding (GIB) rapidly reduces effective blood volume, thereby precipitating acute kidney injury (AKI). Terlipressin, which can induce splanchnic vasoconstriction and increase renal perfusion, has been recommended for acute GIB and hepatorenal syndrome in liver cirrhosis. Thus, we hypothesized that terlipressin might be beneficial for cirrhotic patients with acute GIB and renal impairment. METHODS: In this Chinese multi-center study, 1644 cirrhotic patients with acute GIB were retrospectively enrolled. AKI was defined according to the International Club of Ascites (ICA) criteria. Renal dysfunction was defined as serum creatinine (sCr) > 133 μmol/L at admission and/or any time point during hospitalization. Incidence of renal impairment and in-hospital mortality were the primary end-points. RESULTS: The incidence of any stage ICA-AKI, ICA-AKI stages 1B, 2, and 3, and renal dysfunction in cirrhotic patients with acute GIB was 7.1%, 1.8%, and 5.0%, respectively. The in-hospital mortality was significantly increased by renal dysfunction (14.5% vs. 2.2%, P < 0.001) and ICA-AKI stages 1B, 2, and 3 (11.1% vs. 2.8%, P = 0.011), but not any stage ICA-AKI (5.7% vs. 2.7%, P = 0.083). The in-hospital mortality was significantly decreased by terlipressin in patients with renal dysfunction (3.6% vs. 20.0%, P = 0.044), but not in those with any stage ICA-AKI (4.5% vs. 6.0%, P = 0.799) or ICA-AKI stages 1B, 2, and 3 (0.0% vs. 14.3%, P = 0.326). CONCLUSION: Renal dysfunction increased the in-hospital mortality of cirrhotic patients with acute GIB. Terlipressin might decrease the in-hospital mortality of cirrhotic patients with acute GIB and renal dysfunction. TRIAL REGISTRATION: NCT03846180 ( https://clinicaltrials.gov ).
BACKGROUND:Acute gastrointestinal bleeding (GIB) rapidly reduces effective blood volume, thereby precipitating acute kidney injury (AKI). Terlipressin, which can induce splanchnic vasoconstriction and increase renal perfusion, has been recommended for acute GIB and hepatorenal syndrome in liver cirrhosis. Thus, we hypothesized that terlipressin might be beneficial for cirrhoticpatients with acute GIB and renal impairment. METHODS: In this Chinese multi-center study, 1644 cirrhoticpatients with acute GIB were retrospectively enrolled. AKI was defined according to the International Club of Ascites (ICA) criteria. Renal dysfunction was defined as serum creatinine (sCr) > 133 μmol/L at admission and/or any time point during hospitalization. Incidence of renal impairment and in-hospital mortality were the primary end-points. RESULTS: The incidence of any stage ICA-AKI, ICA-AKI stages 1B, 2, and 3, and renal dysfunction in cirrhoticpatients with acute GIB was 7.1%, 1.8%, and 5.0%, respectively. The in-hospital mortality was significantly increased by renal dysfunction (14.5% vs. 2.2%, P < 0.001) and ICA-AKI stages 1B, 2, and 3 (11.1% vs. 2.8%, P = 0.011), but not any stage ICA-AKI (5.7% vs. 2.7%, P = 0.083). The in-hospital mortality was significantly decreased by terlipressin in patients with renal dysfunction (3.6% vs. 20.0%, P = 0.044), but not in those with any stage ICA-AKI (4.5% vs. 6.0%, P = 0.799) or ICA-AKI stages 1B, 2, and 3 (0.0% vs. 14.3%, P = 0.326). CONCLUSION:Renal dysfunction increased the in-hospital mortality of cirrhoticpatients with acute GIB. Terlipressin might decrease the in-hospital mortality of cirrhoticpatients with acute GIB and renal dysfunction. TRIAL REGISTRATION: NCT03846180 ( https://clinicaltrials.gov ).