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急性肾功能衰竭(ARF)的发病机制自50年代起研究,迄今尚未获得一致意见.下面所述的ARF发病机制,是从不同实验动物模型中所得结果进行讨论,这些实验资料虽然未必能充分阐明临床所见的ARF的发病机理,但可供临床医师在认识和处理ARF时作为参考. 一、返漏学说:应用微穿刺法将~(14)C-菊粉直接注入因缺血或肾动脉内注射硝酸双氧铀而受损的大鼠一侧肾脏的肾小管腔后,可在对侧肾脏生成的尿液内发现有大量放射性菊粉排出,证实了受损肾脏的肾小管上皮细胞有较高的通透性,从而菊粉得以漏出而进入全身血液循环,进而从对侧肾脏排出.所以有人认为,在ARF时肾小管管腔内原尿向肾间质的返漏,一方面使尿量减少,另一方面又因肾间质水肿的形成而压迫肾小管和阻碍原尿通过,结果肾小球囊内压增高,肾小球滤过率(GFR)进一步减少。肾间质水肿又可影响肾小管周围毛细血管内的血液循环,加
The pathogenesis of acute renal failure (ARF) has not been agreed until now since the 1950s.The pathogenesis of ARF, described below, is discussed from the results obtained in different animal models of experiments, although these experimental data may not be fully elucidated Clinical findings of the pathogenesis of ARF, but for clinicians in the understanding and treatment of ARF as a reference. Back to the doctrine: the application of micro-puncture method ~ (14) C-inulin directly into the ischemic or renal artery Intra-injection of uranyl nitrate and impaired rat renal tubules of the kidneys, the urine can be generated in the contralateral kidney with a large number of radioactive inulin excretion confirmed renal tubular epithelial cells There is a higher permeability, so that inulin can leak out into the systemic blood circulation, and then discharged from the contralateral kidney.Therefore, some people think that when the renal tubular endothelium in ARF to the renal interstitial leakage, on the one hand Urine output decreased, on the other hand because of the formation of interstitial edema and the formation of oppression and obstruction of the original urine through the renal capsule, the results of increased glomerular capsule pressure, glomerular filtration rate (GFR) to further reduce. Renal interstitial edema can affect the capillary circulation around the renal tubular blood circulation, plus