虽然对急性肾功能衰竭(ARF)已进行了三、四十年的研究,就其发病机制的病理生理学目前尚不十分清楚。已提出许多学说包括血管学说(血流动力学学说)、肾小管学说和肾小球学说等,然而没有一个学说能解释ARF的所有功能障碍及其发生机制。事实上ARF发病机制是多因素的。就病因而论,缺血型ARF和中毒型ARF的发病机制可以不同;就病程来说。初期(产生期)和持续期的发生机制也可以不同。至于人类ARF和实验性ARF,它们的发病机制也不可能完全相同。已证明ARF与肾脏血流动力学的较大改变有关。肾素-血管紧张素系统(RAS)是调节肾内血流动力学的一个重要体液系统。多数学者已同意ARF实质上是肾小球滤过率(GFR)的减少。而GFR的减少和管球反馈机制的激活很可能是由RAS Although acute renal failure (ARF) has been studied for three to four decades, the pathophysiology of its pathogenesis is not well understood. Many theories have been proposed, including the theory of blood vessels (hemodynamics), tubule theory and glomerular theory, etc. However, no theory can explain all the dysfunction of ARF and its mechanism. In fact, the pathogenesis of ARF is multifactorial. On the etiology, the pathogenesis of ischemic ARF and poisoned ARF can be different; on the course of the disease. The mechanism of initiation (duration) and duration may also vary. As for human ARF and experimental ARF, their pathogenesis may not be exactly the same. ARF has been shown to be associated with major changes in renal hemodynamics. The renin-angiotensin system (RAS) is an important body fluid system that regulates renal hemodynamics. Most scholars have agreed that ARF is essentially a decrease in glomerular filtration rate (GFR). However, the decrease of GFR and the activation of the ball feedback mechanism are likely to be caused by RAS