Kleeman C R, Levi J, Better O
Nephron. 1975;15(3-5):261-78. doi: 10.1159/000180516.
We have presented a review of the interrelationship between the kidney and the adrenocortical steroids, aldosterone and cortisol primarily in the regulation of water and electrolyte metabolism. The presentation is divided into three parts: (1) the influence of cortisol and aldosterone on renal structure and function; (2) the effect of kidney disease on secretion and metabolism of these steroids, and (3) the role of the kidneys in the plasma clearance of these steroids and their metabolites. There is no evidence that an excess or deficit of these steroids have a direct effect on renal structure, but both are necessary to maintain normal GFR and RPF. Glucocorticoids augment renal hemodynamics in pharmacologic doses. The phenomenon of 'escape' by the kidney from the sodium-retaining effect of adrenocortical steroids is discussed in detail, as well as the ability of glucocorticoid to antagonize the sodium retaining activity of any adrenal steroid of analogue with lesser glucocorticoid noperties. It is included that the impaired water dunesis of glycocorticoid deficiency is due to the absence of the permissive action of these steroids on the kidney, augmented at times by enhanced ADH secretion in response to sustained nonosmotic stimuli. The effect of gluco and mineralocorticoids on the renal excretion of divalentions and uric acid is also discussed. While progressive chronic renal failure (CRF) does not seem to significantly after the secretion or metabolism of cortisol it is possible that CRF causes a state of chronic hyperaldosteronism that is essential to maintain normal excretion (secretion) of potassium per nephron as renal mass progressively decreases. A direct or an indirect effect of potassium ion may be responsible for the hypersecretion or aldosterone rather than the renin-angiotensin system.
我们主要就水和电解质代谢的调节，对肾脏与肾上腺皮质类固醇（醛固酮和皮质醇）之间的相互关系进行了综述。该综述分为三个部分：（1）皮质醇和醛固酮对肾脏结构和功能的影响；（2）肾脏疾病对这些类固醇分泌和代谢的影响；（3）肾脏在这些类固醇及其代谢产物血浆清除中的作用。没有证据表明这些类固醇的过量或不足对肾脏结构有直接影响，但两者对于维持正常的肾小球滤过率（GFR）和肾血浆流量（RPF）都是必需的。糖皮质激素在药理剂量下可增强肾脏血流动力学。详细讨论了肾脏对肾上腺皮质类固醇钠潴留作用的“逃逸”现象，以及糖皮质激素拮抗任何具有较低糖皮质激素特性的肾上腺类固醇类似物钠潴留活性的能力。研究认为，糖皮质激素缺乏导致的水代谢障碍是由于这些类固醇对肾脏缺乏允许作用，有时还因对持续非渗透性刺激的抗利尿激素（ADH）分泌增加而加剧。还讨论了糖皮质激素和盐皮质激素对二价离子和尿酸肾脏排泄的影响。虽然进行性慢性肾衰竭（CRF）似乎对皮质醇的分泌或代谢没有显著影响，但随着肾单位数量逐渐减少，CRF可能导致慢性醛固酮增多症状态，这对于维持每个肾单位正常的钾排泄（分泌）至关重要。钾离子的直接或间接作用可能是醛固酮分泌过多的原因，而非肾素 - 血管紧张素系统。
