尽管几个细胞学机制被认为可以阐述脓毒性急性肾损伤(AKI)的机制,AKI发生的病理生理学机制仍然知之甚少。但是至少清楚的是不是一个单一的而是综合性细胞机制对AKI的病因负责。综合这些生理机制一起对肾微循环(MC)进行损害。这就是为什么它被认为是对脓毒症肾MC的反应,探讨其影响因素(DYS)的功能以及它如何导致肾功能衰竭的发病机制。足够的器官 Although several cytological mechanisms are thought to elucidate the mechanism of septic acute kidney injury (AKI), the pathophysiology of AKI remains poorly understood. But at least it is clear that not a single but comprehensive cellular mechanism is responsible for the etiology of AKI. In combination with these physiological mechanisms, renal microcirculation (MC) is compromised. This is why it is considered to be a response to renal MC in sepsis, exploring the function of its influencing factor (DYS) and how it leads to the pathogenesis of renal failure. Enough organs