【摘要】 急性肾脏病(AKD)是新近提出的介于急性肾损伤(AKI)和慢性肾脏病(CKD)之间的一组临床综合征,即AKI 1期或以上持续大于7 d而小于90 d的肾脏损伤。AKD发病与患者年龄、种族、遗传背景、CKD与合并症、急性疾病及AKI的严重程度和持续时间等因素密切相关。AKD发病机制较为复杂,目前认为,CKD与合并症、急性疾病及引起AKD的各种病因可引起肾脏缺血、缺氧共同病理改变,导致肾脏内皮细胞受损、微循环障碍、肾小管细胞G2/M周期停滞和细胞"沉寂"、巨噬细胞等免疫细胞局部募集与活化;多种基因表达异常,特别是生物标记物异常改变,加之衰老、表观遗传等因素,导致炎症因子和细胞因子等异常表达;肾脏局部持续炎症状态,甚至纤维化信号通路激活,肾小管上皮细胞再生能力下降,出现肾脏损伤后"不良修复"和修复延迟;以上机制共同导致AKD发生与进展。因此,了解AKD病因与发病机制对探讨AKI损伤与修复新机制,以及阻断其发展到CKD具有重要理论与防治意义。更多还原

【Abstract】 Acute kidney disease( AKD),a group of clinical syndromes between acute kidney injury( AKI) and chronic kidney disease( CKD),is defined as the kidney injury from after 7 days of AKI to the onset of CKD for 90 days. The pathogenesis of AKD is closely related to multiple factors including age,race,gene,CKD and comorbidities,acute disease,and the severity and duration of AKI. The mechanism of AKD is relatively complex. At present it is considered that CKD and comorbidities,acute diseases,AKD,and other causes can cause renal ischemia,and common pathological changes of hypoxia,leading to renal endothelial cell damage, microcirculation disturbance, tubular cell G2/M cycle stagnation and cell"silence",local recruitment and activation of macrophages and other immune cells,abnormal expression of a variety of genes,and especially abnormal changes of biomarkers. These factors,combining with aging and epigenetics,etc,can contribute to abnormal expression of inflammatory cytokines and cytokines,renal local persistent inflammation,and even activation of fibrosis signal pathway,tubular epithelial cell regeneration impairment,resulting in"poor repair"and repair delay after renal injury. The above mechanisms lead to the occurrence and progression of AKD. Therefore,it is of important theoretical and prevention and treatment significance to understand the etiology and pathogenesis of AKD for exploring new mechanisms of injury and repair of AKI so as to block its progression to CKD.更多还原