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一、生理机制急性肾功能衰竭最终都有肾皮质缺血的改变,所以称“血管运动性肾病”。急性肾小管坏死只是一种组织学的名称,个别急性肾衰病人可发生肾小球无血、轻微或明显的肾小管坏死,局灶性肾小球血栓形成,甚至肾皮质坏死等形态学的改变。Munck与Ruebi等发现休克肾患者肾皮质血流为正常时的22～46％,而近髓肾单位血流为正常值的75％,这时机体的反应是牺牲皮质血运而保存内层肾单位的血流。肾体积可增大到140％,这是损伤的内皮细胞肿胀、远曲小管因管型梗阻而扩张以及间质水肿所致。1977年Levi-
First, the physiological mechanism of acute renal failure eventually have renal cortical ischemia changes, so called “vasomotor nephropathy.” Acute tubular necrosis is only a histological name, some patients with acute renal failure may occur glomerular no blood, slight or obvious tubular necrosis, focal glomerular thrombosis, and even renal cortical necrosis and other morphological change. Munck and Ruebi found that renal blood flow in patients with shock kidney was normal to 22 ~ 46%, while the proximal myeloid unit blood flow was 75% of normal, then the body’s reaction is to sacrifice the cortical blood supply and save the inner kidney Unit of blood flow. Renal volume can be increased to 140%, which is damaged endothelial cell swelling, distal tubule due to tubal obstruction and expansion and interstitial edema caused. 1977 Levi-