Smith I K
Postgrad Med J. 1975 Aug;51(598):506-8. doi: 10.1136/pgmj.51.598.506.
A review of the literature has shown that the role of renin in renal failure is not resolved. It has been invoked as an aggravating factor: decreased renal perfusion releasing large quantities of renin sufficient to cause further renal vasoconstriction. If so, then angiotensin generation and action must occur entirely intrarenally since the vasoconstriction appears to be confined entirely to this vascular bed. It may prove necessary to evaluate the renin-angiotensin system within the kidney rather than peripherally. Elevated renin levels in peripheral plasma are at least as likely to be a consequence of reduced renal perfusion as a cause of it. The few studies so far undertaken of the renin-angiotensin system in renal failure associated with liver disease are inconclusive. If further studies should ascribe a role to renin in the pathology of renal failure, then it may be possible to treat the condition by pharmacological manipulation of the renin-angiotensin system and thereby prevent some of the more serious consequences of renal failure.
文献综述表明,肾素在肾衰竭中的作用尚未明确。它曾被认为是一个加重因素:肾灌注减少会释放大量肾素,足以导致进一步的肾血管收缩。如果是这样,那么血管紧张素的生成和作用必定完全发生在肾脏内部,因为血管收缩似乎完全局限于这个血管床。或许有必要评估肾脏内部而非外周的肾素 - 血管紧张素系统。外周血浆中肾素水平升高至少同样可能是肾灌注减少的结果而非原因。迄今为止,针对与肝病相关的肾衰竭患者肾素 - 血管紧张素系统所开展的少数研究尚无定论。如果进一步的研究认定肾素在肾衰竭病理过程中发挥作用,那么或许可以通过对肾素 - 血管紧张素系统进行药物调控来治疗这种病症,从而预防肾衰竭的一些更为严重的后果。