Hyperaldosteronisim
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Primary hyperaldosteronism is characterized by excessive aldosterone production independent of the renin-angiotensin system, causing hypertension, hypokalemia, and alkalosis in patients not taking diuretics. Over 50% of cases are due to a unilateral adrenal adenoma, while other causes include bilateral adrenal hyperplasia, adrenal carcinoma, and glucocorticoid-remediable aldosteronism. Tests to diagnose include checking electrolytes after withdrawing medications that affect them, finding an increased aldosterone level and normal or high renin level to exclude other diagnoses, and assessing hormone levels in different postures. Treatment depends on the underlying cause, and may include surgery, sp
Hyperaldosteronisim
- 2. Primary hyperatdoteronisim is excess production of aldosterone, independent of renin-angiotensin ‘system. Consider this when the following features are present: hypertension. hypokalaemia, alkalosis in someone not on diuretics. Sodium tends to be mildly raised or normal.
- 3. >50% due to unilateral adrenocortical adenoma (Conn’s syndrome). Also: bilateral adrenocortical hyperplasia: adrenal carcinoma (rare); glucocorticoids- remediable aldosteronism (Or in GRA) In GRA the ACTH regulatory element of the 11 b-hydroxyiase gene fuses to the aldosterone syntheses gene increasing aldosterone production. and bringing it under the control of ACTI. Causes:
- 4. Tests: U & E (when not on diuretics, hypotensives. steroids, K or ‘laxatives for 4 wks): don’t rely on a low K+ (30% are normokalaemic) ↑one and ↓renin – normal or high renin excludes the diagnosis. The differential diagnosis relies on assessing the effect of posture on renin, aldosterone, and cortisol (measure at 9AM lying, and at noon standing). If ↓ cortisol and aldosterone on standing: ACTH - dependents , ie Conn’s or GRA. If ↓cortisol and aldosterone↑ : angotensin II –dependent – ie hyperplasia. Do abdo CT/MRI for primary hyperaldosteronism to localize tumour.
- 5. Seek expert assistance. For (suspect particularly f family history of early hypertension) genetic testing is available. NB renal artery stenos is a more common cause of refractory ↑ BP and ↓K+. Evaluate with renal Dopplers. captopril renogram. or angiography (the gold standard).
- 6. Treatment : Conn’s: Surgery spironolactone up to 300mg/24h po for 4 weeks pre- op Hyperplasi : Spironolactone or amiloride. If GRA is suspected: dexamethasone lmg/24h po for 4 weeks, normalizes biochemistry but not always BP. If BP still ↑, give Spironolactone; stop dexariethasone.
- 7. Secondary hyperaldosteronism: Due to a high renin (eg from renal artery stenosis. accelerated hypertension, diuretics, CCF. hepatic failure.
- 8. Bartter’s syndrome: This is a major cause of congenital (recessive) salt wasting - via a CC leak un the loop of Henle. Presents in childhood with failure to thrive , polyuria, and polydipsia. BP is normal and there is no oedema. Look for hypokalaemia, hyochloraemic metabolk alkalosis, and ↑urinary K+ and Cl- , Plasma, renin ↑. Treatment include K+ replacement, NSAIDs amiloride, captopril.