1/How does primary aldosteronism present? When should you look for it?
Here are a couple of clinical cases I like to share with audiences when I talk about the severity spectrum of primary aldosteronism, and the many ways autonomous aldosterone secretion can manifest.
2/Here are two patients.
3/ Would you screen for primary aldosteronism?
4/
Case 1 = YES. He has chronic HTN, uncontrolled on 4 drugs, and hypoK.
Case 2 = Prob not? This patient would’ve been “normotensive” in the past, but in 2018, he has HTN. His PCP starts him on chlorthalidone and 2 weeks later his K=2.9.
5/ Would you screen Case 2 for primary aldosteronism now?
7/ Both patients are screened for PA, see results.
8/ Could these patients have primary aldosteronism?
9/
Case 1: YES/CONFIRMED. HypoK, suppressed renin, very high aldosterone. This is a positive screen and positive confirmation.
Case 2: YES/POSSIBLY. Normal K. suppressed renin. But ?inappropriately elevated? aldosterone?
10/ Case 2 undergoes a confirmatory oral sodium suppression test (4 days of high sodium diet). 24h UNa>200 mmol and 24h aldosterone excretion rate = 16 mcg/24h
11/
Does Case 2 have primary aldosteronism?
12/
YES, they both have PA.
Case 1 was obvious, prob could have been diagnosed years/decades earlier.
Case 2 was diagnosed early and will hopefully avoid years of CV disease.
13/
Final thoughts:
Exact prevalence not completely clear, but primary aldosteronism can be detected in severe/resistant HTN (>10%), mild-mod HTN (~4-10%)…
Much more work needed to determine how to expand screening in an effective way to detect PA early/end
15/ For more on primary aldosteronism => see final version of our comprehensive, contemporary (and colorful!) review. We review the history of aldosteronism, and the latest in diagnosis, pathogenesis, and treatment...
We characterized the unrecognized severity spectrum of primary aldosteronism
Findings suggest a need to reframe/redefine clinical approaches and terminology to reflect that PA is a common syndrome that can manifest across the blood pressure continuum/1
First - very grateful to be able to work with this stellar team: @JeniferBrown for countless hours of hard work and dedication (and years working to better characterize PA), and the collaborative wisdom of @msiddiqui_, Bob Carey, David Calhoun, Gordon Williams, Paul Hopkins /2
Every participant had physiologic confirmatory testing (oral sodium suppression) regardless of arbitrary screening indications or ARR thresholds
Figs: the magnitude and continuous distribution of non-suppressible, renin-independent, 24h aldosterone production by BP phenotype/3