Ischemic and non-ischemic acute kidney injury cause hepatic damage
Ischemic and non-ischemic acute kidney injury cause hepatic damage
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DOI：
10.1038/ki.2008.683
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发表时间：
2009-04-01
影响因子：
19.6
通讯作者：
Soleimani, Manoocher
中科院分区：
文献类型：
--
作者：
Golab, Fereshteh;Kadkhodaee, Mehri;Soleimani, Manoocher
最近的研究证明，远隔器官会受到肾脏缺血性损伤的影响。在这里，我们研究了在诱导大鼠肾缺血-再灌注期间肝脏是否也受到损害，并将其与双侧肾切除术进行了比较。肝组织肿瘤坏死因子-α水平在肾缺血或肾切除后6小时和24小时显著升高。肾缺血组和肾切除组肝脏中脂质过氧化指标丙二醛升高，总谷胱甘肽降低，提示氧化应激激活。肾缺血或肾切除后6h，肝损伤早期上调的肝精胺-亚精胺乙酰转移酶的表达显著增加。肾切除后24 h，肝细胞凋亡率增加。我们还发现了缺血和双侧肾切除后肝细胞损伤的组织学证据。在肾缺血诱导之前，注射还原型谷胱甘肽显著改善肝脏结构，并与降低肝脏丙二醛和血清丙氨酸转氨酶水平有关。我们的研究表明，急性肾缺血或肾功能衰竭会激活氧化应激，促进肝细胞的炎症、凋亡和组织损伤。
Recent studies have documented that remote organs are affected by ischemic injury to the kidney. Here we studied whether the liver also suffers damage during induction of renal ischemia-reperfusion in rats and compared this to bilateral nephrectomy. Hepatic levels of tumor necrosis factor-alpha increased significantly after 6 and 24 h of renal ischemia or nephrectomy. Malondialdehyde, an index of lipid peroxidation, increased while total glutathione was decreased in the liver in both the renal ischemia and nephrectomy groups, suggesting activation of oxidative stress. Expression of liver spermine-spermidine acetyl transferase, an enzyme upregulated in early phases of hepatic injury was significantly increased 6 h after either kidney ischemia or nephrectomy. Apoptosis was increased in hepatocytes 24 h after nephrectomy. We also found histological evidence of hepatocyte injury following both ischemia and bilateral nephrectomy. Infusion of reduced glutathione, before the induction of renal ischemia, significantly improved liver architecture and was associated with a reduction in hepatic malondialdehyde and serum alanine transaminase levels. Our study shows that acute kidney ischemia or renal failure activates oxidative stress and promotes inflammation, apoptosis, and tissue damage in hepatocytes.