Primary Aldosteronism: Where Are We Now? Where to from Here?

Abstract

The past nine years have seen major advances in establishing the etiology of unilateral primary aldosteronism, and very possibly that of bilateral hyperaldosteronism, in response to somatic mutations in aldosterone synthase expressing cells. Though there have been important advances in the management of primary aldosteronism, in small but convincing studies, they represent minor changes to current guidelines. What has been totally absent is consideration of the public health issue that primary aldosterone represents, and the public policy issues that would be involved in addressing the disorder. In his introduction to PiPA 6, Martin Reincke calculated that only one in a thousand patients in Germany with primary aldosteronism were treated appropriately, an astounding figure for any disease in the 21st century. Towards remedying this totally unacceptable public health issue, the author proposes a radical simplification and streamlining of screening for primary aldosteronism, and the management of most patients by general practitioners. The second bottle-neck in current management is that of mandatory adrenal venous sampling for all but 1–2% of patients, a costly procedure requiring rare expertise. Ideally, it should be reserved – on the basis of likelihood, enhanced imaging, or peripheral steroid profiles – for a small minority of patients with clear evidence for unilateral disease. Only when costs are minimized and roadblocks removed will primary aldosteronism be properly treated as the public health issue that it is.

Prevalence of primary aldosteronism in type 2 diabetes mellitus and hypertension: A prospective study from Western India

“…Even considering screen positive as suppressed renin with aldosterone >10 ng/dl, the prevalence of screen positive in our cohort is 14.4% (70/486). The variability of aldosterone concentrations and posture‐dependent changes have prompted the use of 24‐h urinary aldosterone as a more comprehensive measure of aldosterone secretion as a confirmatory test in all patients with suppressed renin 23,24 . However, we used seated SST as a confirmatory test for convenience only in those with elevated ARR.…”

Normotensive presentation in primary aldosteronism: A report of two cases

“…In recent years, with the widespread use of ARR as a screening test, the prevalence of PA has increased from 0.7% to 29.8%, depending on the population that is selected and the diagnostic values that are used. 2 Currently, some scholars believe that occult hyperaldosteronism constitutes 45%–50% of essential hypertension, of which ⩾90% will be attributable to idiopathic hyperaldosteronism (IHA) 3 ; however, APA has a more evident presentation characterized by marked hypertension, spontaneous hypokalemia, and higher levels of plasma aldosterone. 4 Therefore, it can be speculated that normotensive and normokalemic IHA patients are not rare, although normotensive and hypokalemic patients with APA are even rarer.…”

Development of [18F]AldoView as the First Highly Selective Aldosterone Synthase PET Tracer for Imaging of Primary Hyperaldosteronism

“… 2 Although PHA is a potentially curable cause of secondary hypertension, it is estimated that >99% of those with PHA remain undiagnosed and on lifelong medication at a high cost to individuals and healthcare budgets. 3 In most cases, PHA is due to either bilateral hyperplasia of the adrenal cortex or an aldosterone-producing adenoma (APA). For patients with a demonstrable unilateral cause, surgical removal of the abnormal gland (adrenalectomy) often results in reduced blood pressure, lower dependence on antihypertensive drugs, and sometimes in the complete cure of hypertension (30–60% of cases).…”

“…PHA occurs in 5–10% of patients with hypertension and in 15–25% of those with treatment-resistant hypertension . Although PHA is a potentially curable cause of secondary hypertension, it is estimated that >99% of those with PHA remain undiagnosed and on lifelong medication at a high cost to individuals and healthcare budgets . In most cases, PHA is due to either bilateral hyperplasia of the adrenal cortex or an aldosterone-producing adenoma (APA).…”