Antithrombin III Attenuates AKI Following Acute Severe Pancreatitis. Issue 5 (May 2018)

• Record Type: Journal Article
• Authors: Kong, Yiwei; Yin, Jianyong; Cheng, Dongsheng; Lu, Zeyuan; Wang, Niansong; Wang, Feng; Liang, Mingyu
• Is Part Of: Shock. Volume 49:Issue 5(2018)
• Publication Date: 2018-05
• Subjects: Acute kidney injury -- antithrombin III -- inflammation -- severe acute pancreatitis -- AKI -- acute kidney injury -- ATIII -- antithrombin III -- BUN -- blood urea nitrogen -- ICAM-1 -- intercellular cell adhesion molecule 1 -- MCP-1 -- monocyte chemotactic protein 1 -- MDA -- malondialdehyde -- PAS -- periodic acid–Schiff -- SAP -- severe acute pancreatitis -- Scr -- serum creatinine -- SIRS -- systemic inflammatory response -- SOD -- superoxide dismutase -- TNFα -- tumor necrosis factor α; Shock -- Periodicals; Shock -- Periodicals; Choc (Pathologie) -- Périodiques; Shock; Periodicals; 616.0475
• DOI: 10.1097/SHK.0000000000000946
• Languages: English
• ISSNs: 1073-2322

Abstract

ABSTRACT: Background: Antithrombin III (ATIII), the predominant coagulation factor inhibitor, possesses anti-inflammatory properties and exerts renoprotective effects on renal ischemia-reperfusion injury in animal models. However, the ATIII's protective effects of ATIII on acute kidney injury (AKI) following severe acute pancreatitis (SAP) need to be confirmed. Methods: We assessed the association between ATIII activities and the incidence of AKI in patients with SAP, and explored therapeutic effects and potential mechanisms of ATIII on kidney injury in sodium taurocholate induced SAP rat model. Rats were intravenously injected with ATIII (500 μg/kg) before or after the induction of SAP. Results: The results demonstrated ATIII did not attenuate pancreatic injury, but significantly ameliorate renal dysfunction and renal histological injury. ATIII administration alleviated renal inflammation response, oxidative stress, and cell apoptosis. Moreover, ATIII attenuated tumor necrosis factor α (TNFα)-stimulated intercellular cell adhesion molecule 1(ICAM-1) and monocyte chemotactic protein 1 (MCP-1) upregulation in cultured renal tubular epithelial cells. Conclusion: ATIII appears to ameliorate SAP-induced kidney injury by inhibiting inflammation, oxidative stress, and apoptosis. ATIII supplementation may have a potential prophylactic and therapeutic effect on SAP induced AKI.