Table 3.
Primary hyperaldosteronism | Liddle’s syndrome and variants (renal Na+ channel mutations) | Renal/renovascular | |
---|---|---|---|
Renin | Low** | Low | High |
Aldosterone | High** | Low | High |
Primary treatment | Aldosterone antagonist | Amiloride | Angiotensin receptor blocker *** |
(spironolactone or eplerenone) | |||
Amiloride for men where | (rarely revascularization) | ||
eplerenone is not available | |||
(rarely surgery) |
(Reproduced by permission of Oxford University Press from: Akintunde A, Nondi J, Gogo K, Jones ESW, Rayner BL, Hackam DG, et al. Physiological Phenotyping for Personalized Therapy of Uncontrolled Hypertension in Africa. Am J Hypertens 2017; 30: 923-30.)
It should be stressed that this approach is suitable for tailoring medical therapy in patients with resistant hypertension; further investigation would be required to justify adrenalectomy or renal revascularization.
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.
Angiotensin Converting Enzyme (ACE) inhibitors are less effective because of aldosterone escape via non-ACE pathways such as chymase and cathepsin; renin inhibitors are seldom used.