Endocrine surgery · KIMS Secunderabad
Conn's Syndrome (Primary Hyperaldosteronism) — An Important and Treatable Cause of Resistant Hypertension
Primary hyperaldosteronism (Conn's syndrome) is a condition in which one or both adrenal glands produce excess aldosterone — independently of the renin-angiotensin system that normally regulates aldosterone secretion. The excess aldosterone causes sodium retention (raising blood pressure), potassium wasting (causing hypokalaemia), and suppression of plasma renin. It is the most common cause of secondary hypertension, accounting for 5 to 10% of all hypertensive patients and up to 20% of those with resistant hypertension (blood pressure uncontrolled on three or more antihypertensives).
The clinical importance of identifying primary hyperaldosteronism goes beyond blood pressure control. Excess aldosterone independently damages the heart, kidneys, and blood vessels beyond its pressure-raising effects — causing left ventricular hypertrophy, atrial fibrillation, stroke, and kidney disease at rates significantly higher than in essential hypertension matched for blood pressure. Treatment — either surgical cure by adrenalectomy (for a unilateral aldosterone-producing adenoma, APA) or medical control with aldosterone antagonists (for bilateral hyperplasia) — reverses these risks.
Who should be screened for primary hyperaldosteronism
Hypertension resistant to three or more antihypertensives at adequate doses (including a diuretic)
Hypertension with spontaneous or diuretic-induced hypokalaemia (potassium below 3.5 mEq/L)
Hypertension with an adrenal incidentaloma (any adrenal mass found on imaging)
Hypertension with onset before age 40
Hypertension with a family history of primary hyperaldosteronism or early-onset hypertension
Hypertension with obstructive sleep apnoea
Diagnosis
Aldosterone-to-renin ratio (ARR)
The first-line screening test. Performed on a morning blood sample after the patient has been sitting for 15 minutes. A ratio above 30 (with aldosterone above 15 ng/dL) is a positive screen. Potassium should be corrected before testing. Interfering medications (spironolactone, eplerenone, amiloride) must be stopped 4 weeks before testing; ACE inhibitors, ARBs, and diuretics may affect the result.
Confirmatory testing
A positive ARR requires confirmation to exclude false positives. Standard confirmatory tests: fludrocortisone suppression test (aldosterone fails to suppress with fludrocortisone administration), oral salt loading (aldosterone remains inappropriately high despite sodium loading), or saline infusion test (2 litres IV saline over 4 hours — aldosterone above 5 ng/dL after saline infusion confirms primary hyperaldosteronism).
Adrenal CT
After biochemical confirmation. Identifies unilateral adenoma (APA), bilateral hyperplasia, or an adrenal carcinoma. However, CT alone cannot reliably distinguish APA from bilateral hyperplasia — a normal-appearing adrenal on CT does not exclude a small APA.
Adrenal vein sampling (AVS)
The definitive test to distinguish unilateral (APA — surgical candidate) from bilateral (hyperplasia — medical treatment) primary hyperaldosteronism. Bilateral adrenal vein blood is sampled simultaneously for aldosterone and cortisol. A lateralisation ratio above 4:1 indicates a unilateral source. AVS is recommended before adrenalectomy in all patients above 35 years (younger patients with clear unilateral adenoma on CT may proceed to surgery without AVS). At KIMS, AVS is performed by the interventional radiology team.
Treatment
Unilateral APA — laparoscopic or robotic adrenalectomy
Surgical removal of the adenoma-bearing adrenal gland cures hypertension in 35 to 70% of patients and significantly improves blood pressure control in the remainder, reducing antihypertensive requirements. Hypokalaemia resolves within days of surgery. Aldosterone normalises immediately post-operatively. Robotic adrenalectomy at KIMS by Dr. Likhiteswer Pallagani — day-care or 1-night stay.
Bilateral hyperplasia — medical management
Spironolactone (a competitive aldosterone antagonist) or eplerenone (selective mineralocorticoid receptor antagonist — fewer anti-androgenic side effects) normalise potassium and significantly reduce blood pressure. Blood pressure improvement on spironolactone alone is substantial — many patients reduce or eliminate other antihypertensives. Amiloride is an alternative in patients who cannot tolerate spironolactone.
Book a Hypertension and Adrenal Assessment at KIMS
Frequently Asked Questions — Conn's Syndrome
Primary hyperaldosteronism affects 5 to 10% of all hypertensive patients — far more common than most clinicians appreciate. In resistant hypertension (blood pressure uncontrolled on three or more antihypertensives), the prevalence rises to 15 to 20%. This means that in a city like Hyderabad with millions of hypertensive adults, tens of thousands have undiagnosed primary hyperaldosteronism that is causing not just resistant hypertension but aldosterone-driven cardiovascular damage — all of which is treatable once the diagnosis is made. The ARR screening test is simple, inexpensive, and should be performed in every patient with resistant hypertension.
Yes — excess aldosterone independently increases the risk of stroke, atrial fibrillation, and left ventricular hypertrophy beyond what can be explained by blood pressure elevation alone. Aldosterone has direct toxic effects on the cardiovascular system: it promotes cardiac fibrosis, endothelial dysfunction, inflammation, and vascular remodelling. Studies consistently show that patients with primary hyperaldosteronism have higher rates of cardiovascular events — stroke, atrial fibrillation, myocardial infarction — than patients with essential hypertension matched for the same blood pressure. This is why identifying and treating primary hyperaldosteronism matters beyond just controlling blood pressure.
In patients with a unilateral aldosterone-producing adenoma treated by adrenalectomy, hypertension is cured (off all antihypertensives, normal blood pressure) in approximately 35 to 70% of cases. The remainder achieve significant improvement — lower blood pressure on fewer medications. Cure rates are higher in younger patients, those with shorter duration of hypertension, those without a family history of hypertension, and those with lower pre-operative ARR. The hypokalaemia resolves in essentially all cases. Even in patients not fully cured, the elimination of excess aldosterone reduces the ongoing cardiovascular damage and reduces antihypertensive medication burden significantly.
Spironolactone is the most effective medical treatment for bilateral primary hyperaldosteronism but has anti-androgenic side effects from its non-selective action: gynaecomastia (breast tissue growth in men — in up to 10% of patients on high doses), reduced libido, and menstrual irregularities in women. These are dose-dependent and often manageable by using the lowest effective dose. Eplerenone — a selective mineralocorticoid receptor antagonist — has significantly fewer anti-androgenic effects and is preferred for patients who develop gynaecomastia or sexual side effects on spironolactone. Potassium levels must be monitored on both agents.
KIMS Secunderabad — Dr. Likhiteswer Pallagani (robotic adrenalectomy), aldosterone-to-renin ratio testing, confirmatory saline infusion test, CT adrenal, adrenal vein sampling coordination with interventional radiology, robotic adrenalectomy for unilateral APA, spironolactone and eplerenone protocol for bilateral hyperplasia. NABH and NABL accredited. Call 040-4488-5000.