HOW TO TREAT 31
ausdoc. com. au 31 OCTOBER 2025
HOW TO TREAT 31
17-alpha-hydroxylase
Pregnenolone 17-OH-pregnenolone
Androgens
3-hydroxysteroid dehydrogenase
Progesterone
17-alpha-hydroxylase 17-OH-progesterone
21-hydroxylase Deoxycorticosterone
21-hydroxylase
11-Deoxycorticosterone
11-beta-hydroxylase Corticosterone
11-beta-hydroxylase Cortisol
Aldosterone
Figure 8. Adrenal steroidogenesis pathway.
lesion with low Hounsfield units suggestive of a lipid-rich adrenal adenoma. Further hormonal testing with a 1mg dexamethasone suppression test excluded cortisol excess.
Simon subsequently underwent adrenal vein sampling, which was consistent with bilateral excess aldosterone production. Medical treatment with spironolactone, an MRA, was started at 25mg daily and prazosin was stopped. Spironolactone was increased to 37.5mg daily at the subsequent clinic visit three months later with good effect. At follow-up six months later, his blood pressure was less than 130 / 80mmHg and plasma renin concentration was greater than 15mU / L.
This case illustrates bilateral adrenal hyperplasia as a cause of PA, presenting as LRH. The adrenal lesion is likely a non-functioning adrenal adenoma, a common incidental radiological finding that should not be taken as an indicator of unilateral aldosterone excess.
Case study two
Lydia, a 33-year-old woman, consults her GP for a repeat prescription of the combined oral contraceptive pill( OCP). This is the only medication she is taking. There is no family history of hypertension or cardiovascular disease.
On examination, she has a mean clinic blood pressure of 168 / 102mmHg and a BMI of 28.5kg / m 2. The GP diagnoses hypertension. There are no clinical signs of glucocorticoid or androgen excess. Her initial investigations appear in table 4.
At a follow-up visit Lydia and her GP discuss her results. After a discussion and counselling regarding alternative contraceptive options, Lydia stops taking the OCP. Her repeat renin and aldosterone measurements appear in table 4.
This case highlights the OCP as a cause of a false positive ARR, as it can reduce renin and increase aldosterone concentrations. 42 Repeat testing is warranted after cessation.
ARR≥70
D / D: Primary aldosteronism
Consider referral to an endocrinologist( or empirical treatment with spironolactone if specialist access is not available)
No
Check aldosterone
Case study three
Anna, a 49-year-old woman, presents to her GP complaining of muscle cramps. Her medical history
Low renin + hypertension
Interfering factors?( see table 1)
Yes
Yes
Consider re-evaluation
ARR < 70
Red flags: Young age + family history, features of cortisol or androgen excess
|
Figure 9. A suggested approach to the management of low renin hypertension.
* Only Moduretic, a combination of amiloride and hydrochlorothiazide, is currently available on the PBS.
|
D / D: Cushing’ s syndrome, NC-CAH, DOC-secreting tumour, AME, Liddle syndrome, Gordon syndrome,
MR activating mutation
Consider referral to endocrinologist or nephrologist
|
D / D LREH
Consider empirical treatment with spironolactone or thiazides( or amiloride *)
|
AME: apparent mineralocorticoid excess, |
|
|
CAH: congenital adrenal hyperplasia, D / D: differential diagnosis, DOC: deoxycorticosterone, LREH: low-renin essential hypertension, |
MR: mineralocorticoid receptor, MRA: MR antagonist, NC-CAH: non-classical congenital adrenal hyperplasia, PA: primary aldosteronism. |
Table 4. Lydia’ s initial investigations and follow-up results Investigation and reference range
Lydia’ s initial results
Potassium mmol / L( 3.5-5.2) 3.9 3.8 Plasma renin concentration mU / L( 4.4-46) 6.5 22.5 Aldosterone pmol / L( 70-1090) 543 240 ARR pmol / mU( less than 70) 84 11
Lydia’ s followup results
is significant for dyslipidaemia and vitamin D insufficiency. Her only medication is cholecalciferol 1000 units daily. There is no family
No
history of hypertension or cardiovascular disease.
Physical examination reveals a mean clinic blood pressure of 178 / 102mmHg and a heart rate of 84bpm. Her BMI is 31kg / m 2. Her initial investigations appear in table 5.
Given her severe hypokalaemia, the GP refers her to the nearest ED for inpatient management.
In hospital, her ECG is unremarkable, and the hypokalaemia is corrected with IV potassium chloride and subsequently oral potassium replacement. Further history
Table 5. Anna’ s initial investigations
Investigation and reference range
Potassium mmol / L( 3.5-5.2)
Calcium, corrected mmol / L( 2.10-2.60)
Magnesium mmol / L( 0.7-1.1)
Phosphate mmol / L( 0.75-1.50)
Creatinine μmol / L( 50-100)
Plasma renin concentration mU / L( 4.4-46)
Aldosterone pmol / L( 70-1090)
Anna’ s initial results
2.4
2.35
0.90
0.98
75
< 2
45
Table 6. Anna’ s repeat investigations
Investigation and reference range
Potassium mmol / L( 3.5-5.2)
Plasma renin concentration mU / L( 4.4-46)
Aldosterone pmol / L( 70-1090)
Random cortisol at 9.20PM nmol / L( 185- 625)*
Adrenocorticotrophin hormone pmol / L( less than 10)
24-hour urine cortisol excretion nmol / day( 60-310)
Anna’ s initial results
3.6
Less than 2
53
111
3.1
212
TSH mIU / L( 0.4-4.8) 3.6
Free thyroxine pmol / L( 8.0-16.0)
9.8
* Reference interval for morning cortisol. Evening cortisol levels are approximately 50 % lower.