Hyperadosteronism

Question 1

What is the epidemiology of hyperaldosteronism?

Answer 1

F>M
Most common in 30-50yrs
c.5-10% prevalence

The most common and curable form of secondary HTN

Question 2

What is the aetiology and pathophysiology of hyperaldosteronism?

Answer 2

Conn’s syndrome:
- Solitary, unilateral mineralocorticoid producing renal adenoma (>80% of cases)

Bilateral adrenal hyperplasia (BAH):
- Adrenal hyperplasia (15% of cases)

(also a familial variant as well as a carcinoma instead of an adenoma)

Excessive aldosterone increases reabsorption of Na and excretion of K

• Cl follows the Na and together create high intravascular salt content - HTN
• Elevated BP will increase GFR which will decrease renin and subsequently angiotensin 2 - this will NOT however be reflected by a drop in aldosterone

Question 3

How does hyperaldosteronism present?

Answer 3

Often asymptomatic

Classic features:

• HTN
• Hypokalaemia (though many patients are normo)
• Metabolic acidosis
• Na on the high end of normal/raised

Other signs of electrolyte imbalance:

• Hypokalaemia = weakness, fatigue, polyuria, cramps, shallow breathing, metabolic alkalosis
• Hypernatraemia = thirst, fatigue, confusion, muscle twitches/spasms, HTN, shock

Question 4

How do you investigate hyperaldosteronism?

Answer 4

Screening for it is important for those with HTN who:

• Present with hypokalaemia
• Resistant HTN
• FHx of adrenal mass

U+E:

• Hypokalaemia
• Hypernatraemia

Random aldosterone + renin levels:

• Aldosterone = raised
• Renin = low (if high, this excludes primary hyperadlosteronism)

ECG:
- May show arrhythmmias

Imaging:
- CT - to confirm a mass or hyperplasia; MRI used second line if doubt as mor sensitive

Selective adrenal venous sampling
- Gold standard for localising the sources of hyperaldosteronism

Question 5

What are some other tests for hyperaldosteronism?

Answer 5

Lying and standing renin levels:

• Aldosterone is affected by upright posture and therefore samples are taken lying down and then repeated after being upright for a few hours
• In general, in primary hyperaldosteronism due to hyperplasia, the plasma aldosterone increases after four hours of standing, usually by more than 30%
• There is usually no alteration in renin/aldosterone levels with posture in the presence of an adrenal adenoma
• These are only guidelines and thus lying/standing levels need to be interpreted with caution, taking into account the patient’s history and the results of imaging investigations

Salt loading and aldosterone/renin levels:

• Patient loaded with sald for 2wks before samples
• Salt should suppress plasma aldosterone
• Aldosterone:renin, cortisol and bicarbonate levels taken
• Failure to suppress confirms primary hyperaldosteronism

Aldosterone:renin ratio:

• Screening tool for patients with (resistant) HTN and hypokalaemia
• Ratio >800 and patients should be investigated

check with your local centre, as some will still perform salt loading and lying/standing renin/aldosterone levels.

Question 6

How do you manage hyperaldosteronism?

Answer 6

Conn’s:
- Laparoscopic adrenalectomy -for adenoma/carcinoma

BAH:
Spironolactone or eplerenone 
- For people with bilateral hyperplasia 
- Aldosterone antagonists 
Amiloride 
- K sparing diuretic to counteract hypokalaemia; but doesnt have mineralocorticoid inhibition

Question 7

What are some causes of secondary hyperaldosteronism?

Answer 7

Diuretics

Congestive cardiac failure

Hepatic failure

Nephrotic syndrome

RAS

Malignant hypertension

Investigations and treatment should be directed towards the underlying cause