Physiologically individualised therapy for resistant hypertension based on phenotyping by plasma renin activity and aldosterone
| Primary hyperaldosteronism (usually due to bilateral adrenocortical hyperplasia) | Liddle phenotype (mutations of ENac and of other genes affecting the function of ENac) | Renal/renovascular | |
| Renin | Low* | Low | High |
| Aldosterone | High* | Low | High |
| Primary treatment | Aldosterone antagonist (spironolactone or eplerenone) Amiloride for men where eplerenone is not available (rarely surgery)‡ | Amiloride | Angiotensin receptor blocker or renin inhibitor† (rarely revascularisation) |
*Levels of plasma renin and aldosterone must be interpreted in the light of the medication the patient is taking at the time of sampling. In a patient taking an angiotensin receptor blocker (which would elevate renin and lower aldosterone), a plasma renin that is in the low normal range for that laboratory, with a plasma aldosterone in the high normal range, probably represents primary hyperaldosteronism, for the purposes of adjusting medical therapy.
†ACE inhibitors are less effective because of aldosterone escape via non-ACE pathways such as chymase and cathepsin.
‡It should be stressed that this approach is suitable for tailoring medical therapy in resistant hypertensives; further investigation would be required to justify adrenalectomy or renal revascularisation.
(Reproduced with permission from Elsevier: Spence30).