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非特异性急性肾功能衰竭的病理生理迄今仍未明确。有两种主要看法,一种强调肾小管坏死,另一种则强调肾血管收缩是肾衰的主要原因。本文主要从动物模型和人的观察来分析这些看法。动物模型的观察在大鼠和狗,用多种肾毒素(如重铬酸盐、硝酸双氧铀及汞),用甘油造成肌肉损伤,血红蛋白尿和正铁血红蛋白尿,暂时阻塞肾动脉以及由肾内输入血管收缩剂等,已能诱发急性肾功能衰竭。但这些资料并不说明任何一个因素是肾衰的“唯一”原因。在肾毒性或缺血后引起的急性肾衰中,有充分证据说明滤过液可通过损伤的肾小管上皮回漏。正常肾小管不能透过的大分子物质如菊粉(分子量为
The pathophysiology of nonspecific acute renal failure has not been elucidated so far. There are two main ideas, one emphasizes tubular necrosis, the other emphasizes that renal vasoconstriction is the main cause of renal failure. This article analyzes these observations mainly from animal models and human observations. Animal models were observed in rats and dogs with various nephrotoxins (such as dichromate, uranyl nitrate and mercury), muscle damage with glycerol, hemoglobinuria and methemoglobineuria, temporary obstruction of the renal arteries and by the kidneys Entering vasoconstrictors, etc., has been able to induce acute renal failure. However, these data do not indicate that any one factor is the “only” cause of renal failure. In acute renal failure caused by nephrotoxicity or ischemia, there is good evidence that filtration fluid can leak back through damaged renal tubular epithelium. Normal tubules can not permeate macromolecules such as inulin (molecular weight