Post liver transplantation acute kidney injury in a rat model of syngeneic orthotopic liver transplantation

被引:9
作者
Wang, Jun [1 ]
Du, Zhiyong [2 ]
Zhang, Wen [1 ]
Han, Baosan [2 ]
Peng, Chenghong [2 ]
Chen, Nan [1 ]
机构
[1] Shanghai Jiao Tong Univ, Sch Med, Ruijin Hosp, Dept Nephrol, Shanghai 200025, Peoples R China
[2] Shanghai Jiao Tong Univ, Sch Med, Ruijin Hosp, Dept Surg, Shanghai 200025, Peoples R China
关键词
acute kidney injury; inflammation; liver transplantation; macrophage; peritubular capillary; renal tubule; ENDOTHELIAL GROWTH-FACTOR; REPERFUSION INJURY; RENAL DYSFUNCTION; ISCHEMIA; DAMAGE; CELLS; PRESERVATION; EXPRESSION; INITIATION; RECOVERY;
D O I
10.1038/labinvest.2011.59
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Acute kidney injury (AKI) is a frequent complication after liver transplantation (LT). The mechanism of post-LT AKI remains unclear. We used the rat model of syngeneic orthotopic LT (SOLT) to investigate the mechanism of post-LT AKI. We hypothesized that the condition of the graft, rather than intraoperative hemodynamic instability, has an important role in post-LT AKI in the SOLT model. Rats were randomly assigned into four groups: sham-operated group; vessel-clamped group; full-size LT group; and reduced-size LT group. We identified AKI in both full-size and reduced-size LT groups. In addition to renal tubular necrosis and apoptosis, renal peritubular capillary injury was also present. Pathological changes were more severe in the reduced-size than in the full-size LT group. We found that the systemic inflammatory response induced by LT was the initiating factor in post-LT AKI. This is the first study to investigate the pathological mechanism of AKI in an animal model of SOLT. Our results demonstrate that protection of the liver graft and inhibition of the systemic inflammatory response are vital in reducing the risk of post-LT AKI. Laboratory Investigation (2011) 91, 1158-1169; doi:10.1038/labinvest.2011.59; published online 23 May 2011
引用
收藏
页码:1158 / 1169
页数:12
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