HyperaldosteronisimHyperaldosteronisim

Primary hyperatdoteronisim is excess Primary hyperatdoteronisim is excess production of aldosterone, production of aldosterone,

independent of renin-angiotensin ‘system. independent of renin-angiotensin ‘system.

Consider this when the following features Consider this when the following features are present: hypertension.are present: hypertension.

hypokalaemia, alkalosis in someone not on hypokalaemia, alkalosis in someone not on diuretics. diuretics.

Sodium tends to be mildly raised or Sodium tends to be mildly raised or normal.normal.

>50% due to unilateral adrenocortical adenoma >50% due to unilateral adrenocortical adenoma (Conn’s syndrome). (Conn’s syndrome).

Also: Also: bilateral adrenocortical hyperplasia: bilateral adrenocortical hyperplasia: adrenal carcinoma (rare); adrenal carcinoma (rare); glucocorticoids- remediable aldosteronism (Or glucocorticoids- remediable aldosteronism (Or

in GRA) In GRA the ACTH regulatory in GRA) In GRA the ACTH regulatory element of the 11 b-hydroxyiase gene fuses element of the 11 b-hydroxyiase gene fuses to the aldosterone syntheses gene increasing to the aldosterone syntheses gene increasing aldosterone production. aldosterone production.

and bringing it under the control of ACTI.and bringing it under the control of ACTI.

Causes: Causes:

Tests:Tests: U & E (when not on diuretics, hypotensives. U & E (when not on diuretics, hypotensives. steroids, K or ‘laxatives for 4 wks): don’t rely on a low steroids, K or ‘laxatives for 4 wks): don’t rely on a low

K+ (30% are normokalaemic) ↑one and ↓renin – K+ (30% are normokalaemic) ↑one and ↓renin – normal or high renin excludes the diagnosis. normal or high renin excludes the diagnosis.

The differential diagnosis relies on assessing the effect The differential diagnosis relies on assessing the effect of posture on renin, aldosterone, and cortisol of posture on renin, aldosterone, and cortisol (measure at 9AM lying, and at noon standing). (measure at 9AM lying, and at noon standing).

If ↓ cortisol and aldosterone on standing: If ↓ cortisol and aldosterone on standing: ACTH - dependents , ie Conn’s or GRA. ACTH - dependents , ie Conn’s or GRA. If ↓cortisol and aldosterone↑ : angotensin II –If ↓cortisol and aldosterone↑ : angotensin II –

dependent – ie hyperplasia. dependent – ie hyperplasia. Do abdo CT/MRI for primary hyperaldosteronism to Do abdo CT/MRI for primary hyperaldosteronism to

localize tumour. localize tumour.

Seek expert assistance. Seek expert assistance.

For (suspect particularly f family history of For (suspect particularly f family history of early hypertension) genetic testing is early hypertension) genetic testing is available. available.

NB renal artery stenos is a more common NB renal artery stenos is a more common cause of refractory ↑ BP and ↓K+.cause of refractory ↑ BP and ↓K+.

Evaluate with renal Dopplers. captopril Evaluate with renal Dopplers. captopril renogram. renogram.

or angiography (the gold standard).or angiography (the gold standard).

TreatmentTreatment: : Conn’s: Conn’s: Surgery spironolactone up to 300mg/24h po Surgery spironolactone up to 300mg/24h po

for 4 weeks pre- op Hyperplasi : for 4 weeks pre- op Hyperplasi : Spironolactone or amiloride. Spironolactone or amiloride.

If GRA is suspected: If GRA is suspected: dexamethasone lmg/24h po for 4 weeks, dexamethasone lmg/24h po for 4 weeks, normalizes biochemistry but not always BP. normalizes biochemistry but not always BP. If If BP still ↑, BP still ↑, give Spironolactone; give Spironolactone; stop stop dexariethasone.dexariethasone.

Secondary hyperaldosteronism:Secondary hyperaldosteronism:

Due to a high renin (eg from renal artery Due to a high renin (eg from renal artery stenosis.stenosis.

accelerated hypertension, accelerated hypertension,

diuretics, diuretics,

CCF. CCF.

hepatic failure.hepatic failure.

Bartter’s syndrome:Bartter’s syndrome: This is a major cause of congenital (recessive) saltThis is a major cause of congenital (recessive) saltwasting - via a CC leak un the loop of Henle. wasting - via a CC leak un the loop of Henle. Presents in childhood with failure to thrive , Presents in childhood with failure to thrive , polyuria, polyuria, and polydipsia. and polydipsia. BP is normal and there is no oedema. BP is normal and there is no oedema. Look for hypokalaemia, hyochloraemic metabolk Look for hypokalaemia, hyochloraemic metabolk

alkalosis, and ↑urinary K+ and Cl- , alkalosis, and ↑urinary K+ and Cl- , Plasma, Plasma, renin ↑. renin ↑. Treatment include K+ replacement, NSAIDs Treatment include K+ replacement, NSAIDs

amiloride, captopril.amiloride, captopril.