Padfield P L
Department of Medical Sciences, Western General Hospital, University of Edinburgh, Scotland, UK.
J Hum Hypertens. 2002 Mar;16(3):159-62. doi: 10.1038/sj.jhh.1001321.
Primary aldosterone excess or hyperaldosteronism is an important cause of hypertension which, when associated with an aldosterone secreting adenoma, is amenable to surgical cure. The biochemical hallmarks of the condition are a relative excess of aldosterone production with suppression of plasma levels of renin (a proxy for angiotensin II, the major trophic substance regulating aldosterone secretion). This combination of a high aldosterone and a low renin is however more commonly associated with 'nodular hyperplasia' of the adrenal glands, a condition not improved by surgery and variably responsive to the effects of the mineralocorticoid antagonist, spironolactone. Until recently the prevalence of either form of secondary hypertension has been thought to be low such that few clinicians 'hunted' for it in the absence of hypokalaemia (the traditional clue for the syndrome). This view has been challenged, firstly by the realisation that no more than 50% of such patients will have a low plasma potassium and secondly by the assumption that a 'normal' plasma aldosterone is in fact inappropriately elevated if the renin level is low. A single measurement of the ratio of aldosterone to renin levels is claimed to be highly predictive of patients who will have primary aldosterone excess. This paper examines the logic behind such claims and presents evidence from the literature that an abnormal ratio is simply a different description of the low renin state and that such patients do not necessarily have mineralocorticoid hypertension. Most patients 'discovered' by this test will have what many call low-renin hypertension, a condition not amenable to specific therapy. Claims that they are peculiarly sensitive to the hypotensive effects of spironolactone have not been tested in controlled trials. The test would however be expected to pick up those individuals with true Conn's syndrome but such patients remain too few in number to justify widespread use of an expensive screening test.
原发性醛固酮增多症或醛固酮增多症是高血压的一个重要病因，当与醛固酮分泌性腺瘤相关时，可通过手术治愈。该病症的生化特征是醛固酮产生相对过多，同时血浆肾素水平受到抑制（肾素是血管紧张素II的替代指标，血管紧张素II是调节醛固酮分泌的主要营养物质）。然而，高醛固酮和低肾素的这种组合更常见于肾上腺“结节性增生”，这种情况手术无法改善，且对盐皮质激素拮抗剂螺内酯的效果反应不一。直到最近，人们一直认为这两种继发性高血压的患病率都很低，以至于在没有低钾血症（该综合征的传统线索）的情况下，很少有临床医生去“追查”它。这种观点受到了挑战，首先是因为认识到此类患者中不超过50%会出现低血钾，其次是因为如果肾素水平低，那么“正常”的血浆醛固酮实际上是不适当升高的。单次测量醛固酮与肾素水平的比值据称对患有原发性醛固酮增多症的患者具有高度预测性。本文探讨了此类说法背后的逻辑，并展示了文献中的证据，即异常比值仅仅是低肾素状态的另一种描述，而且此类患者不一定患有盐皮质激素性高血压。通过该检测“发现”的大多数患者会患有许多人所说的低肾素性高血压，这种病症无法进行特异性治疗。关于他们对螺内酯的降压作用特别敏感的说法尚未在对照试验中得到验证。然而，该检测有望找出那些真正患有康恩综合征的个体，但此类患者数量仍然太少，无法证明广泛使用昂贵的筛查检测是合理的。
