“Aldosterone Escape” or Refractory Hyperaldosteronism?

To the Editor,

The term “aldosterone escape” has been used to refer to 2 distinct phenomena that are exactly opposite each other: (1) escape from the sodium-retaining effects of excess mineralocorticoids or aldosterone in primary hyperaldosteronism,[1–3] which is a manifestation of volume and/or pressure natriuresis, and (2) the inability of angiotensin-converting enzyme (ACE) inhibitor therapy to reliably suppress aldosterone release, for example, in patients with heart failure or diabetes.[4–6] In the latter situation, aldosterone escape is associated with increased salt and water retention. I wish to introduce the term “refractory hyperaldosteronism” to refer to the failure of ACE inhibitor or angiotensin receptor blocker therapy to suppress aldosterone release as it directs attention to factors other than angiotensin II (for example, plasma potassium levels), which influence aldosterone release. However, we could retain the current use of the term “aldosterone escape” to refer to escape from the salt-retaining effects of excess aldosterone, as occurs in primary hyperaldosteronism.

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