• Great progress have been made in our understanding of the
pathophysiology of PA syndrome since Conn’s description of
the clinical presentation of a patient with an aldosterone-
d i d th
producing adenoma more than 50 years ago.
Hyper-aldosteronism: Should we check on it in all
hypertensive patients • Although most clinicians had thought PA to be a rare form of
HTN for more than three decades, it is now recognized to be the
Ahmed El Hawary MD most common form of secondary HTN.
Suez Canal University
• Using the plasma aldosterone to plasma renin activity ratio as
a case-finding test, followed by aldosterone suppression
Prevalence: evolving recognition
confirmatory testing, has resulted in much higher prevalence
estimates of 5–13% of all patients with HTN. • In the past, clinicians would not consider the diagnosis of PA
• Although thought to be complex in the past, the diagnostic
g g p p , g unless the patient presented with spontaneous hypokalaemia.
approach to primary aldosteronism is straightforward and can
• This diagnostic approach resulted in predicted prevalence rates
be considered in three phases:
of less than 0·5% of hypertensive patients.
1. Case-finding tests
2. Confirmatory tests
3. Subtype evaluation tests
Prevalence: evolving recognition
• The diagnosis of PA is usually made in patients who are in the
• However, it is now recognized that most patients with PA are third to sixth decade of life.
not hypokalaemic and that screening can be completed with a
• Few symptoms are specific to the syndrome.
simple blood test [plasma aldosterone concentration (PAC) to
plasma renin activity (PRA) ratio].
l i ti it ti ] • Patients with marked hypokalaemia may have muscle weakness
and cramping, headaches, palpitations, polydipsia, polyuria,
• Using the PAC:PRA ratio as a case-finding test, followed by nocturia, or a combination of these.
aldosterone suppression confirmatory testing, has resulted in
• The polyuria and nocturia are a result of hypokalaemia-induced
much higher prevalence of PA (5–13% of all patients with HTN).
renal concentrating defect and the presentation is frequently
mistaken for prostatism in men.
Clinical presentation Clinical presentation
• There are no specific physical findings. • Patients with PA have higher risk than other patients with HTN for
TOD of the heart and kidney.
• Oedema in not a common finding because of ‘mineralocorticoid
escape’. • When matched for age, BP, and duration of HTN, patients with PA
have greater LV mass, higher rate of CV events (e.g. stroke, AF and
The d f i ll d t t
• Th degree of HTN is usually moderate to severe.
MI) than essential HTN patients.
• HTN may be resistant to usual pharmacological treatments.
• Arterial wall stiffness is higher in PA compared to essential HTN.
• Because of a reset osmostat, the serum sodium tends to be high-
• PA patients had a higher urinary albumin excretion rate than
normal or slightly above the upper limit of normal. This clinical
comparable patients with essential HTN.
clue is very useful when initially assessing the potential for PA.
1. Case-finding testing
3. Subtype studies
• Adrenal CT.
• Adrenal venous sampling.
2·2-cm right adrenal
nodule (arrow) on
When to consider testing for PA
1. HTN and hypokalaemia (regardless of presumed cause).
2. Resistant HTN (three antihypertensive drugs and poor control).
3. Severe HTN (≥ 160 systolic or ≥ 100 diastolic).
4. HTN and an incidental adrenal mass.
5. Onset of HTN at a young age (<50 years of age).
6. Patients evaluated for other forms of secondary HTN.
7. Evidence of TOD, particularly if disproportionate for the
severity of HTN.