急性肾损伤（AKI）是ICU常见病。研究证实AKI即使完全恢复，仍是慢性肾病（CKD）的危险因素，但AKI向CKD转化的机制至今不详。我们前期研究发现脓毒症相关AKI恢复期存在不良修复，以炎症细胞渗出、上皮细胞周期停滞为主。MaR1可调节腹腔炎症细胞渗出、促进腹腔巨噬细胞向M2转化并增强其吞噬功能。而研究表明M2型巨噬细胞在I/R和白喉毒素所致AKI模型中可促进修复并抑制纤维化。据此我们提出假设，MaR1可通过调节炎症细胞渗出，促进肾脏巨噬细胞向M2转化，从而抑制脓毒症相关AKI向CKD转化。本实验建立小鼠盲肠结扎穿孔术（CLP）诱导的脓毒症相关AKI恢复期模型，采用免疫印迹，免疫荧光，Q-PCR，流式等方法，研究MaR1对肾脏巨噬细胞向M2分化的影响及巨噬细胞表型转化对脓毒症相关AKI向CKD转化的影响。为脓毒症相关AKI恢复期治疗提供新策略。

Acute kidney injury (AKI) is a common disease among ICU patients. It has been demonstrated that AKI, even complete recovery, is still a risk factor for chronic kidney disease(CKD). However, the mechanism of AKI to CKD progression is not well understood. Our preliminary data showed that maladaptive repair was activated after acute phase, however, the process was mainly composed by inflammatory cells infiltration and tubular epithelial cell cycle arresting. MaR1 regulated inflammatory cells infiltration, promoted peritoneal macrophage polarized into M2 and enhanced phagocytosis. Previous study also demonstrated that M2 phenotype of macrophage promoted repair process and attenuated fibrosis in I/R or Diphtheria toxin(DT)-induced AKI model. Hence, we propose the hypothesis that, MaR1 might inhibit sepsis-associated AKI to CKD progression by regulating inflammatory cells infiltration and promote macrophage to polarize into M2. In this study, we will establish cecum ligation and puncture( CLP) induced sepsis-associated AKI with progression to CKD model, and explore the effects of MaR1 on renal macrophage polarizing into M2 as well as the effects of macrophage phenotype on sepsis-associated AKI with progression to CKD by western blotting, immunofluorescence, Q-PCR, flow, et. This study will provide new therapeutic strategy for sepsis-associated AKI with progression to CKD.