
Contents
Introduction
- As opposed to Cushing’s Syndrome – which is an excess of glucocorticoids, and as opposed to Addison’s disease which is a lack of both glucocorticoids and aldosterone
Causes
- About 80% of cases are due to a solitary mineralocorticoid producing adrenal adenoma.
- Classically this is “Conn’s Syndrome” and other causes technically are not. In reality, the terms hyperaldosteronism and Conn’s syndrome are often used interchangeably
- About 20% of cases are due to adrenal hyperplasia.
- 15% of cases are bilateral
- <5% of cases are unilateral
- Adrenal carcinoma can also cause hyperaldosteronism
Pathology
Presentation
- Hypertension
- Hypokalaemia
- 70% of patients have normal potassium
- May cause weakness
- Hypernatraemia
- Most patients have sodium in the normal range
- Metabolic alkalosis
- Polyuria and polydipsia
Investigations
- U+E – may show hypernatraemia and hypokalaemia – but often not
- Renin and aldosterone levels
- Increased aldosterone
- Decreased renin – if renin is normal then primary aldosteronism is excluded
- Aldosterone/renin ratio is the usual way that diagnosis is confirmed
- Ratio >800 confirms diagnosis and prompts need to investigate for the cause
- Results can be altered by antihypertensives
- False positives – B-blockers
- False negatives – ACE-inhibitors, ARBs, calcium channel blockers
- ECG – signs of hypokalaemia
- CT / MRI
- To look for adrenal mass or hyperplasia
- Salt loading and renin and aldosterone levels
- Patients are loaded with salt tablets and high salt diet for two weeks
- In the normal physiological state, this should suppress plasma aldosterone
- In primary hyperaldosteronism, aldosterone is not suppressed
- Rarely used – doesn’t seem to enhance diagnostic rate and is fiddly and time-consuming
- Lying and standing aldosterone and renin levels
- Can differentiate between adrenal hyperplasia and adrenal adenoma
- Samples taken after lying down for several hours and repeated after standing for several hours
- Need careful interpretation by a specialist
- In adrenal hyperplasia – aldosterone increases after 4 hours of standing by >30%
- In adrenal adenoma – there is not change in postural results
Differentials
There are many possible differentials, although clinically the most important is renal artery stenosis (RAS) which often presents with a similarly hypertensive patient. In these circumstances, performing an USS of the renal tract is important to exclude RAS as a differential. Other findings in RAS include:
- Raised renin AND aldosterone
- Renal arteriogram is the gold standard of diagnosis
- U+E may show hypokalaemia and impaired renal function
Other differentials include:
- Cushing’s disease
- Aldosterone and renin levees are low
- Congenital adrenal hyperplasia
- Nephrotic syndrome
Management
- Adrenal adenoma (Conn’s Syndrome)
- Surgical removal of the adenoma
- In the meantime, medical management may be required:
- Spironolactone (aldosterone antagonist)
- Hypertension may persist after removal of tumour due to secondary effects of hypertension on the vasculature
- Bilateral adrenal hyperplasia
- Medical management with aldosterone antagonists
- Spironolactone – blocks both aldosterone and testosterone receptors, which can cause gynaecomastia, menstrual irregularities and erectile dysfunction
- Amiloride – another potassium sparing diuretic, although its effects are generally weaker than spironolactone
- Eplerenone – selective aldosterone antagonist and thus does not suffer from the same testosterone effects as spironolactone. More evidence is needed to evaluate its effectiveness in adrenal hyperplasia
- Medical management with aldosterone antagonists
References
- Hyperaldosteronism - patient.info
- Murtagh’s General Practice. 6th Ed. (2015) John Murtagh, Jill Rosenblatt
- Oxford Handbook of General Practice. 3rd Ed. (2010) Simon, C., Everitt, H., van Drop, F.