Aldosteronism with hyperplasia of the adrenal cortex means your adrenal glands (small glands that sit on top of the kidneys) have grown more cells than normal in the outer layer (the cortex). Those extra cells make too much aldosterone, a salt-regulating hormone. Too much aldosterone tells your kidneys to keep sodium and water and to waste potassium. This raises blood pressure and can lower potassium levels. The problem starts in the adrenal glands themselves (so it is primary aldosteronism), not because of another illness. In most people with hyperplasia, both adrenal glands are involved, and the renin level in blood becomes low because the body senses too much salt and water. OUP Academic+1
Aldosteronism with hyperplasia of the adrenal cortex means the adrenal glands make too much aldosterone because both adrenal glands are a little bigger and overactive (this is called bilateral adrenal hyperplasia). Aldosterone is a hormone that tells the kidneys to hold on to salt (sodium) and let go of potassium. When the body makes too much aldosterone, the blood keeps too much salt and water. This raises blood pressure and can lower potassium. People may have headaches, muscle cramps, weakness, more urination, and high blood pressure that is hard to control. Over many years, too much aldosterone can injure the heart, blood vessels, kidneys, and brain. The diagnosis uses a simple screening blood test (aldosterone-renin ratio), followed by confirmatory tests. Treatment aims to block aldosterone’s effects, lower the blood pressure, restore potassium, and protect the heart and kidneys.
Other names
Doctors use several terms for this same condition:
Bilateral adrenal hyperplasia (BAH)
Idiopathic hyperaldosteronism (IHA) or Idiopathic adrenal hyperplasia (IAH)
Bilateral hyperaldosteronism (BHA)
Primary aldosteronism due to hyperplasia
All of these mean both adrenal glands are overactive and enlarged in a subtle way, making too much aldosterone. PMC+2primaryaldosteronism.org+2
Types
Bilateral diffuse adrenal hyperplasia (classic IHA): Widespread thickening of the outer adrenal layer in both glands with continuous aldosterone production. CT scans may look normal or only slightly “bumpy.” primaryaldosteronism.org
Bilateral micronodular hyperplasia: Many tiny nodules scattered in both glands, each making aldosterone. These nodules can be hard to see on routine imaging. PMC
Unilateral adrenal hyperplasia (rare): Only one gland is hyperplastic; the other is normal. This is uncommon but can mimic an adenoma; adrenal-vein sampling helps tell them apart. NCBI
Familial hyperaldosteronism with hyperplasia: In several inherited forms (see causes below), both glands become overactive because of gene changes that drive aldosterone production. OUP Academic
Causes
Each “cause” below is a driver or contributor known to push adrenal cells to grow or to make aldosterone autonomously. Some are genetic, some are cellular signaling problems, and some are modifiers that worsen the condition.
KCNJ5 gene variants (familial type III and some hyperplastic nodules): Change an ion channel so sodium leaks in, the cell depolarizes, calcium surges, and aldosterone genes turn on. In families, both glands often enlarge and overproduce aldosterone. AhA Journals
CACNA1D gene variants: Alter a calcium channel (Cav1.3), letting more calcium enter adrenal cells and pushing aldosterone synthesis; commonly found in bilateral micronodular hyperplasia clusters. Nature
CLCN2 gene variants (familial type II): Change a chloride channel, depolarize the cell membrane, and stimulate aldosterone production bilaterally. OUP Academic
ATP1A1 or ATP2B3 variants: Disturb sodium/potassium pump or calcium pump balance, leading to chronic depolarization and aldosterone overproduction; can be seen in hyperplastic tissue as well as adenomas. PMC
CACNA1H variants (familial type IV): Affect T-type calcium channels; patients may present young with bilateral disease and very high aldosterone. OUP Academic
Wnt/β-catenin pathway activation: Growth signals that encourage expansion of aldosterone-producing cell clusters (APCCs) and nodular hyperplasia. Frontiers
Aldosterone-producing cell clusters (APCCs) expansion with age: Small clusters accumulate somatic mutations (often CACNA1D), expand, and can create multifocal hyperplasia. Nature
Chronic ACTH sensitivity in zona glomerulosa: In some people, aldosterone-making cells stay abnormally responsive to ACTH, promoting growth and hormone output. OUP Academic
Family history of primary aldosteronism (FH-I to FH-IV): Several inherited patterns cause bilateral aldosterone excess; some are glucocorticoid-remediable (FH-I), others are not. OUP Academic
High dietary salt as a disease amplifier: Does not cause PA by itself, but worsens blood pressure injury and potassium loss once aldosterone is high, driving harmful remodeling. ScienceDirect+2eshonline.org+2
Obstructive sleep apnea (OSA) as a comorbidity/driver: OSA and PA often coexist; sympathetic surges and RAAS changes may aggravate aldosterone excess and resistant hypertension. OUP Academic+1
Metabolic syndrome/obesity: Associated with higher aldosterone activity and resistant hypertension; can interplay with OSA and salt sensitivity to worsen hyperaldosteronism. PMC
Low renin state that persists: Once aldosterone is autonomous from the adrenals, renin suppression removes feedback “brakes,” letting aldosterone stay high chronically. OUP Academic
Micronodular remodeling after long-standing hypertension: Adrenal cortices can develop multiple hormone-active micronodules that behave like a field defect. PMC
Adrenal stem/progenitor cell dysregulation: Early evidence suggests abnormal renewal programs in the cortex may favor aldosterone-secreting cell expansion. Frontiers
Chronic potassium loss loops: Aldosterone causes kaliuresis; hypokalemia then further stimulates aldosterone synthase expression in some settings, reinforcing hypersecretion. PMC
Subtle inflammation/oxidative stress in adrenal cortex: May enhance steroidogenic enzyme expression and growth signaling in hyperplastic tissue. Frontiers
Genetic mosaicism within adrenal tissue: Different nodules within the same person can carry different aldosterone-driver mutations, creating a multifocal hyperplasia pattern. PMC
Developmental variants of zona glomerulosa: Some people have a broader or more active aldosterone zone, predisposing to hyperplasia. Frontiers
Secondary contributors that unmask PA (not causes but reveal it): Diuretics, pregnancy, or severe stress can expose hidden aldosterone excess by lowering potassium or altering volume—revealing the underlying hyperplasia. NCBI
Common symptoms and signs
High blood pressure that is hard to control: Often needs several medicines; sometimes found in younger people than typical essential hypertension. NCBI
Headaches or pounding sensation: From persistently high pressure. PMC
Muscle weakness or tiredness: Low potassium makes muscles less excitable, causing weakness and fatigue. NCBI
Muscle cramps or spasms: Hypokalemia and alkalosis can trigger painful cramps. NCBI
Pins-and-needles or tingling feelings: Nerves can misfire when potassium is low. NCBI
Frequent urination and night-time urination: Kidneys lose potassium and have trouble concentrating urine, causing polyuria and nocturia. PMC
Excess thirst: Goes along with frequent urination. PMC
Heart palpitations or fluttering: Low potassium can trigger abnormal heart rhythms. MSJ Online
Periodic paralysis (rare): Sudden episodes of severe weakness due to very low potassium. NCBI
Numbness around the mouth or in limbs: Electrolyte shifts can cause sensory changes. NCBI
Mood changes or irritability: Electrolyte imbalance and uncontrolled BP can affect mood and sleep. PMC
Low potassium on routine tests without a clear reason: A common lab clue that prompts screening. (Note: many PA patients are not hypokalemic.) NCBI
Resistant hypertension plus sleep apnea symptoms: Snoring, apneas, and daytime sleepiness often coexist and should raise suspicion. PubMed
Metabolic alkalosis on blood tests: Because aldosterone increases hydrogen ion loss. Medscape
Eye changes from long-term high BP (retinopathy) found in exam: A consequence of prolonged pressure exposure. PMC
Diagnostic tests
A) Physical examination (bedside checks)
Accurate blood pressure measurement (both arms, repeated): Confirms sustained or resistant hypertension; seated and standing readings help assess volume and medication effects. OUP Academic
Orthostatic vitals (lying to standing): Looks for volume expansion (often no significant drop) and helps distinguish other causes of hypertension. OUP Academic
Neuromuscular exam (manual muscle testing): Screens for proximal muscle weakness from hypokalemia. NCBI
Fundoscopic exam: Checks for hypertensive retinopathy, signaling long-standing pressure burden. PMC
Anthropometrics and OSA clues (neck circumference, crowded oropharynx): Resistant hypertension plus OSA features heighten suspicion for PA. PubMed
B) “Manual” or functional bedside tests
Home/office serial BP tracking: Multiple readings over days show persistence and treatment resistance, supporting the need to screen for PA. OUP Academic
Ambulatory blood pressure monitoring (24-hour): Documents nocturnal hypertension or non-dipping patterns common in secondary hypertension. PMC
Medication review with test preparation: Temporarily adjusting drugs (eg, holding MR antagonists) lowers false positives before lab screening. Athens Pediatric Clinic
C) Laboratory & pathological tests (the core of diagnosis)
Plasma aldosterone concentration (PAC): Measures aldosterone level; in PA it is inappropriately high for the sodium status. PMC
Renin (plasma renin activity or direct renin concentration): Usually suppressed in PA because the body senses volume expansion. PMC
Aldosterone-to-renin ratio (ARR): Most sensitive screening test; a high ratio suggests PA and triggers confirmatory testing (cut-offs depend on assay). Endocrine Society+1
Serum electrolytes and bicarbonate: Low potassium and elevated bicarbonate (alkalosis) support mineralocorticoid excess but can be normal in many patients. NCBI
24-hour urinary aldosterone (often with sodium loading): After eating extra salt (dietary or tablets), aldosterone should suppress; in PA it stays high. PMC
Saline infusion test (IV suppression): Two liters of saline over 4 hours should lower aldosterone in healthy physiology; failure to suppress supports PA. OUP Academic
Fludrocortisone suppression test (FST): A stricter confirmatory test over several days; less commonly used because it is intensive but very informative. OUP Academic
Captopril challenge test: An oral ACE-inhibitor test; in PA, aldosterone often fails to drop appropriately. OUP Academic
Genetic testing when familial PA is suspected: Looks for FH-I (CYP11B1/B2 chimeric gene) and other familial variants (eg, CLCN2, KCNJ5, CACNA1H/D) in early-onset or family clusters. OUP Academic
Pathology after surgery (selected cases): If tissue is removed for another reason, histology shows diffuse or nodular hyperplasia rather than a single adenoma. (Most BAH is treated medically.) OUP Academic
D) Electrodiagnostic tests (electrical recordings helpful in PA)
Electrocardiogram (ECG): Hypokalemia can cause T-wave flattening/inversion, ST depression, U-waves, and QT/QU prolongation—clues to mineralocorticoid-driven potassium loss. Life in the Fast Lane • LITFL+1
Holter or ambulatory ECG monitoring: Detects intermittent arrhythmias (eg, ectopy, atrial tachyarrhythmias) triggered by low potassium or BP swings. MSJ Online
E) Imaging (to support subtype decisions—not to diagnose PA)
Adrenal CT scan: First-line imaging to look for large masses and to plan veins for sampling. In bilateral hyperplasia, CT can look normal or only mildly thickened. OUP Academic
Adrenal MRI (alternative when CT is unsuitable): Helpful when iodinated contrast is contraindicated; may still miss small hyperplastic nodules. Medscape
Adrenal vein sampling (AVS)—the lateralization gold standard: A catheter study comparing aldosterone from each adrenal; similar levels on both sides suggest bilateral hyperplasia and medical therapy. NCBI
11C-Metomidate PET-CT (specialized centers): A functional scan targeting enzymes used in aldosterone synthesis; studied as a noninvasive aid to subtype PA when AVS is difficult. Lippincott Journals+2Nature+2
Screen with ARR → confirm with a suppression test → image adrenals → localize with AVS if surgery is contemplated. In bilateral hyperplasia, surgery is usually not the answer; doctors typically use a mineralocorticoid-receptor blocker (spironolactone or eplerenone). OUP Academic
Non-pharmacological treatments (therapies & others)
1) Reduced-sodium diet
Description: A low-sodium eating plan means limiting added salt and choosing foods with less sodium. Aim for about 1,500–2,000 mg sodium per day, or what your clinician advises. This means cooking at home more often, tasting food before salting, using herbs, lemon, garlic, pepper, and spices for flavor, and choosing fresh or frozen foods instead of canned or processed items. It also helps to rinse canned beans and vegetables and to read labels to pick lower-sodium options.
Purpose: Lower blood pressure and reduce aldosterone’s harmful effects.
Mechanism: Less sodium intake reduces fluid retention. This lowers blood volume and blood pressure, decreasing the stimuli that worsen aldosterone-mediated strain on the heart and kidneys.
2) DASH-style eating pattern
Description: The DASH (Dietary Approaches to Stop Hypertension) eating style focuses on vegetables, fruits, whole grains, legumes, nuts, low-fat dairy, lean proteins, and minimal added sugars and saturated fats. It complements salt reduction and provides potassium, magnesium, calcium, and fiber that support healthy blood pressure. It is flexible and can be adapted to cultural foods.
Purpose: Improve blood pressure, support potassium balance, and reduce cardiovascular risk.
Mechanism: High-fiber, mineral-rich foods improve vascular function and help the kidneys regulate sodium and water. This lowers blood pressure and counters aldosterone’s vascular effects.
3) Weight management
Description: Achieving and maintaining a healthy weight through balanced nutrition and physical activity lowers blood pressure and reduces medication needs. Even a 5–10% weight loss can help. Sustainable habits include planning meals, portion awareness, strength training, and regular movement you enjoy.
Purpose: Reduce blood pressure and improve insulin sensitivity and heart health.
Mechanism: Lower adiposity reduces sympathetic tone and vascular resistance, improves endothelial function, and reduces aldosterone drive associated with obesity.
4) Regular aerobic activity
Description: Aim for at least 150 minutes per week of moderate-intensity exercise, such as brisk walking, cycling, or swimming, spread over most days. Start slowly if you are new to exercise and increase gradually. Combine this with daily light activity, like taking the stairs and short walking breaks.
Purpose: Lower blood pressure and improve heart and vascular health.
Mechanism: Aerobic exercise improves endothelial function, reduces arterial stiffness, and supports favorable neurohormonal balance, countering aldosterone-related vascular changes.
5) Resistance training
Description: Two to three days per week of whole-body strength work (machines, free weights, or bands) builds lean muscle and supports healthy metabolism. Keep proper form, breathe normally, and avoid straining.
Purpose: Support blood pressure control, glucose handling, and body composition.
Mechanism: More muscle mass increases insulin sensitivity, lowers inflammation, and supports better overall hemodynamics.
6) Sleep optimization
Description: Aim for 7–9 hours of consistent sleep. Create a sleep routine: regular bedtime, quiet dark room, no heavy late meals, limited caffeine late in the day, and reduced screen time before bed. Consider evaluation for sleep apnea if you snore, stop breathing at night, or wake unrefreshed.
Purpose: Improve blood pressure regulation and daytime energy.
Mechanism: Good sleep lowers sympathetic activity and stress hormones that interact with the renin-angiotensin-aldosterone system (RAAS).
7) Stress-reduction training (mindfulness/CBT)
Description: Mindfulness, breathing exercises, and cognitive-behavioral skills lower stress and anxiety. Brief daily practice (5–10 minutes) plus longer sessions when possible helps. Counseling or digital CBT programs can teach coping skills.
Purpose: Reduce stress-related blood pressure spikes.
Mechanism: Lower sympathetic tone and cortisol may blunt stimuli that otherwise amplify aldosterone’s vascular effects.
8) Alcohol moderation
Description: If you drink, follow medical advice (many people with hypertension benefit from avoiding alcohol). If allowed, keep intake very low (for many, ≤1 standard drink/day; some may be advised to avoid completely).
Purpose: Prevent alcohol-related blood pressure increases and arrhythmias.
Mechanism: Lower alcohol reduces sympathetic activation, improves sleep, limits atrial fibrillation risk, and supports BP control.
9) Tobacco cessation
Description: Avoid cigarettes and smokeless tobacco. Use counseling, nicotine replacement, or prescribed cessation medicines if needed.
Purpose: Protect arteries and the heart; improve BP control.
Mechanism: Stopping nicotine reduces vasoconstriction, arterial stiffness, and inflammation that compound aldosterone’s effects.
10) Potassium-rich whole foods (if approved)
Description: With clinician approval and careful lab monitoring, eat potassium-rich foods (e.g., bananas, oranges, potatoes, tomatoes, leafy greens, beans). Not all patients qualify—people with low kidney function or on certain drugs must avoid excess potassium.
Purpose: Help correct aldosterone-related potassium loss.
Mechanism: Dietary potassium supports intracellular balance and can help lower BP by improving vascular tone and sodium handling.
11) Magnesium-adequate diet
Description: Include nuts, seeds, legumes, whole grains, and greens. Magnesium supports muscle and nerve function and helps blood pressure.
Purpose: Support vascular function and reduce cramps.
Mechanism: Magnesium helps calcium handling in vessels and muscle, aiding relaxation and possibly lessening aldosterone-related cramps.
12) Limiting ultra-processed foods
Description: Ultra-processed foods often contain hidden sodium, sugars, and additives that worsen BP. Choose minimally processed staples and cook more at home.
Purpose: Reduce hidden salt and improve nutrient density.
Mechanism: Less sodium and better nutrient profile support lower BP and counter aldosterone’s fluid-retaining effects.
13) Hydration balance
Description: Drink enough fluids for normal thirst and urine color (pale yellow) unless your clinician advises otherwise. Avoid excessive fluids that may worsen blood pressure.
Purpose: Maintain steady volume without overload.
Mechanism: Balanced hydration supports kidney function and stable BP without stimulating aldosterone further.
14) Caffeine awareness
Description: Caffeine can cause short-term BP rises. Track your response and limit strong coffee/energy drinks if you notice spikes or palpitations.
Purpose: Avoid unnecessary BP elevations.
Mechanism: Less adrenergic stimulation helps keep vascular tone stable.
15) Home blood-pressure monitoring
Description: Use a validated arm cuff. Check at the same times daily, seated, after five minutes of rest. Record readings to share with your clinician.
Purpose: Guide therapy and track progress.
Mechanism: Frequent, accurate readings help adjust treatments that counter aldosterone’s effects.
16) Fall-safe activity planning
Description: When potassium runs low, cramps or weakness may occur. Arrange safe movement routines, warm-ups, and stretching. Seek prompt care for severe weakness.
Purpose: Prevent injury during symptomatic periods.
Mechanism: Gentle, planned movement avoids sudden strain on muscles affected by electrolyte shifts.
17) Kidney-protective habits
Description: Avoid unnecessary NSAIDs, stay hydrated as advised, and monitor labs as scheduled.
Purpose: Preserve kidney function that can be stressed by aldosterone excess.
Mechanism: Less nephrotoxic exposure and steady fluid status protect kidneys.
18) Heart-healthy day plan
Description: Create a daily checklist: low-sodium meals, walk, meds on time, stress break, and bedtime routine.
Purpose: Turn treatment goals into repeatable habits.
Mechanism: Consistency reinforces BP control and hormone balance.
19) Education and shared decision-making
Description: Learn your condition, test plan, and options. Bring questions, keep a med list, and know warning signs.
Purpose: Improve adherence and outcomes.
Mechanism: Understanding boosts engagement and timely care.
20) Family screening awareness
Description: Some cases have familial patterns. Encourage close relatives with resistant hypertension or early strokes to get checked.
Purpose: Early detection saves organs.
Mechanism: Screening finds cases before complications appear.
Drug treatments
1) Spironolactone
Description: Spironolactone is a classic mineralocorticoid receptor (MR) antagonist that blocks aldosterone at its receptor. It lowers blood pressure, raises potassium, and protects the heart and kidneys in primary aldosteronism.
Class: MR antagonist (potassium-sparing).
Typical dosing/time: Often 12.5–25 mg once daily to start; titrated (for some, divided dosing).
Purpose: Reduce aldosterone’s actions and control BP.
Mechanism: Competitive blockade of MR in kidney and other tissues reduces sodium reabsorption and potassium loss, lowering volume and BP.
Side effects: High potassium, breast tenderness or enlargement, menstrual changes, GI upset, dizziness. Rarely, rash or severe hyperkalemia.
2) Eplerenone
Description: Eplerenone is a more selective MR antagonist with lower risk of sex-hormone-related side effects. It can be used when spironolactone isn’t tolerated or as initial therapy.
Class: MR antagonist.
Typical dosing/time: Often 25 mg once or twice daily at start; titrated to effect.
Purpose: Block aldosterone effects while minimizing endocrine side effects.
Mechanism: Selective MR blockade reduces sodium retention and potassium wasting.
Side effects: High potassium, dizziness, low BP, kidney function changes; needs lab monitoring.
3) Amiloride
Description: Amiloride is a potassium-sparing diuretic that blocks epithelial sodium channels (ENaC) in the kidney. It is useful if MR antagonists are not tolerated.
Class: ENaC blocker (potassium-sparing).
Typical dosing/time: Commonly 5–10 mg once or twice daily.
Purpose: Lower BP and correct potassium loss.
Mechanism: Inhibits ENaC in the distal nephron, reducing sodium reabsorption and potassium loss driven by aldosterone.
Side effects: High potassium, nausea, dizziness; monitor potassium and kidney function.
4) Chlorthalidone
Description: Chlorthalidone is a long-acting thiazide-like diuretic often used together with MR antagonists to improve BP control.
Class: Thiazide-like diuretic.
Typical dosing/time: 12.5–25 mg once daily, usually morning.
Purpose: Additional BP lowering.
Mechanism: Reduces sodium reabsorption in the distal tubule, decreasing volume and vascular resistance.
Side effects: Low potassium (offset by MR antagonists), low sodium, dizziness, glucose or uric acid changes.
5) Hydrochlorothiazide (HCTZ)
Description: A commonly used thiazide diuretic for hypertension adjunct therapy.
Class: Thiazide diuretic.
Typical dosing/time: 12.5–25 mg once daily.
Purpose: Add-on BP control with MR blockers.
Mechanism: Blocks sodium reabsorption in distal tubules, lowering volume and resistance.
Side effects: Electrolyte changes (low potassium/sodium), photosensitivity, fatigue.
6) Amlodipine
Description: A dihydropyridine calcium channel blocker that relaxes arteries and is often combined with MR antagonists.
Class: CCB (dihydropyridine).
Typical dosing/time: 5–10 mg once daily.
Purpose: Reduce vascular resistance and BP.
Mechanism: Inhibits L-type calcium channels in vascular smooth muscle, causing vasodilation.
Side effects: Ankle swelling, flushing, headache, gingival overgrowth.
7) Nifedipine ER
Description: Another dihydropyridine CCB option for add-on BP control.
Class: CCB.
Typical dosing/time: 30–90 mg once daily (extended-release).
Purpose: Improve BP when MR antagonists alone are not enough.
Mechanism: Arterial vasodilation by calcium channel blockade.
Side effects: Headache, flushing, edema, palpitations.
8) Losartan
Description: An angiotensin II receptor blocker (ARB) useful for BP control and organ protection.
Class: ARB.
Typical dosing/time: 50–100 mg daily (once or split).
Purpose: Lower BP and protect kidneys and heart.
Mechanism: Blocks AT1 receptors, reducing angiotensin II effects that interact with aldosterone signaling.
Side effects: Dizziness, kidney function changes, high potassium (especially with MR antagonists).
9) Valsartan
Description: Another ARB with strong BP-lowering effects; often used when additional RAAS control is needed.
Class: ARB.
Typical dosing/time: 80–320 mg daily (once or split).
Purpose: BP reduction and end-organ protection.
Mechanism: AT1 receptor blockade reduces vasoconstriction and aldosterone stimulation.
Side effects: Dizziness, high potassium risk, kidney function shifts.
10) Lisinopril
Description: An ACE inhibitor that reduces formation of angiotensin II.
Class: ACE inhibitor.
Typical dosing/time: 10–40 mg once daily.
Purpose: Lower BP and protect heart/kidneys.
Mechanism: Inhibits ACE, decreasing angiotensin II and aldosterone drive.
Side effects: Cough, high potassium, kidney changes; rare angioedema.
11) Enalapril
Description: Another ACE inhibitor choice for combination BP therapy.
Class: ACE inhibitor.
Typical dosing/time: 5–40 mg/day (once or twice).
Purpose: Reduce BP and RAAS overactivity.
Mechanism: Lowers angiotensin II and downstream aldosterone stimulation.
Side effects: Cough, hyperkalemia, dizziness; rare angioedema.
12) Carvedilol
Description: A beta-blocker with alpha-blocking activity used when rate control or heart protection is needed (e.g., coronary disease, heart failure history).
Class: Nonselective beta-blocker/alpha-blocker.
Typical dosing/time: 6.25–25 mg twice daily (varies).
Purpose: Support BP and heart protection.
Mechanism: Reduces heart rate and vasoconstriction; lowers adrenergic drive that can interact with RAAS.
Side effects: Fatigue, dizziness, low heart rate, glucose masking.
13) Metoprolol succinate
Description: A beta-1 selective blocker helpful for comorbid heart disease.
Class: Beta-1 blocker.
Typical dosing/time: 25–200 mg once daily (ER).
Purpose: Reduce BP and cardiac workload.
Mechanism: Lowers heart rate/contractility and sympathetic tone.
Side effects: Fatigue, dizziness, low heart rate.
14) Doxazosin
Description: An alpha-1 blocker used as an add-on for resistant BP or when prostate symptom relief is also desired.
Class: Alpha-1 blocker.
Typical dosing/time: 1–8 mg once daily.
Purpose: Lower vascular resistance.
Mechanism: Blocks alpha-1 receptors in vessels, causing vasodilation.
Side effects: Dizziness, first-dose hypotension, fatigue.
15) Hydralazine
Description: A direct vasodilator reserved for resistant hypertension.
Class: Vasodilator.
Typical dosing/time: Often 25–100 mg two to three times daily.
Purpose: Additional BP lowering when others are insufficient.
Mechanism: Direct smooth-muscle relaxation in arterioles lowers resistance.
Side effects: Headache, palpitations, fluid retention, rare lupus-like syndrome.
16) Minoxidil (oral)
Description: A potent arteriolar vasodilator for severe resistant hypertension under close supervision.
Class: Vasodilator (K-channel opener).
Typical dosing/time: Low doses titrated; often with diuretic and beta-blocker.
Purpose: Last-line BP reduction.
Mechanism: Opens ATP-sensitive potassium channels in vascular smooth muscle, causing vasodilation.
Side effects: Fluid retention, tachycardia, hair growth, pericardial effusion (rare).
17) Indapamide
Description: A thiazide-like diuretic alternative to chlorthalidone.
Class: Thiazide-like diuretic.
Typical dosing/time: 1.25–2.5 mg once daily.
Purpose: Add-on BP control.
Mechanism: Inhibits distal tubular sodium reabsorption, lowers volume.
Side effects: Electrolyte shifts, dizziness.
18) Verapamil SR
Description: A non-dihydropyridine CCB that can help in select patients, especially if rate control is desired.
Class: CCB (non-dihydropyridine).
Typical dosing/time: 120–240 mg once or twice daily (SR).
Purpose: Lower BP and heart rate.
Mechanism: Blocks cardiac and vascular L-type channels, reducing rate and resistance.
Side effects: Constipation, bradycardia, edema, drug interactions.
19) Diltiazem ER
Description: Another non-dihydropyridine CCB option.
Class: CCB.
Typical dosing/time: 120–360 mg daily (ER).
Purpose: BP and rate control.
Mechanism: Calcium channel blockade in heart/vessels.
Side effects: Bradycardia, edema, fatigue.
20) Finerenone (specialist use)
Description: A newer, non-steroidal MR antagonist used primarily in chronic kidney disease with diabetes; in select situations and with specialist guidance, MR antagonism beyond spironolactone/eplerenone may be considered.
Class: Non-steroidal MR antagonist.
Typical dosing/time: Dose individualized; requires close potassium/renal monitoring.
Purpose: Additional MR blockade in specific contexts.
Mechanism: Selective MR antagonism reducing fibrosis/inflammation pathways.
Side effects: Hyperkalemia, kidney function changes.
Note: Always follow individualized, FDA-label-based dosing and monitoring as directed by your clinician. Drug choices differ by kidney function, potassium level, pregnancy status, interactions, and co-conditions.
Dietary molecular supplements
1) Potassium (dietary, not pills unless prescribed)
Description: Emphasize food sources (bananas, oranges, potatoes, tomatoes, beans, leafy greens). Some patients must avoid supplements; others may benefit under close monitoring.
Dose: Food-based intake per diet plan; supplements only if prescribed.
Function: Replaces potassium wasted by aldosterone.
Mechanism: Restores cellular and electrical balance, supports normal muscle and heart function, and may help lower BP by improving sodium handling.
2) Magnesium
Description: Many adults do not meet magnesium needs. Foods include nuts, seeds, legumes, whole grains, and greens. Supplements may help cramps and mild BP effects.
Dose: Often 200–400 mg elemental magnesium/day if advised.
Function: Supports muscle/nerve function and vascular relaxation.
Mechanism: Modulates calcium channels and nitric oxide pathways, aiding vasodilation and BP stability.
3) Omega-3 fatty acids (EPA/DHA)
Description: Fish oil or high-EPA/DHA foods (fatty fish).
Dose: Common supplement 1–2 g/day EPA+DHA if approved.
Function: Cardiovascular support and mild BP benefit.
Mechanism: Improves endothelial function, reduces inflammation, and may lower arterial stiffness.
4) Coenzyme Q10
Description: A mitochondrial cofactor sometimes used for adjunct BP support and statin-related muscle symptoms.
Dose: 100–200 mg/day if advised.
Function: Antioxidant and energy support.
Mechanism: Supports mitochondrial electron transport and may improve endothelial nitric oxide activity.
5) L-arginine (or L-citrulline)
Description: Amino acids that support nitric oxide production.
Dose: L-arginine ~3–6 g/day; L-citrulline ~1–3 g/day if appropriate.
Function: Promote vasodilation.
Mechanism: Substrate for nitric oxide synthase, improving vascular relaxation.
6) Vitamin D
Description: Low vitamin D is common; repletion may help overall cardiometabolic health.
Dose: Based on blood level; often 800–2,000 IU/day (or as prescribed).
Function: Bone and immune support; possible BP effects.
Mechanism: Modulates RAAS and inflammation, though BP effects are modest.
7) Beetroot (dietary nitrate)
Description: Beetroot juice/powder can support short-term BP reductions in some people.
Dose: Varies; commonly 250–500 mL juice or 500 mg–2 g powder before activity.
Function: Vasodilation support.
Mechanism: Dietary nitrate → nitric oxide pathway improves endothelial function.
8) Garlic extract
Description: Some formulations show small BP reductions.
Dose: Standardized aged garlic per product (often 600–1,200 mg/day).
Function: Adjunct BP support.
Mechanism: May enhance nitric oxide and reduce vasoconstriction.
9) Taurine
Description: An amino sulfonic acid with potential modest BP effects.
Dose: Often 1–3 g/day if appropriate.
Function: Vascular and autonomic balance support.
Mechanism: May reduce sympathetic tone and improve endothelial signaling.
10) Probiotics (select strains)
Description: Gut-heart axis support; small BP effects reported with multi-strain products.
Dose: Per label (e.g., ≥10^9 CFU/day).
Function: Metabolic and inflammatory tone support.
Mechanism: Short-chain fatty acid production and cytokine modulation may aid vascular health.
Drugs for immunity booster / regenerative / stem-cell related
1) Erythropoietin-stimulating agents (conceptual, 100 words)
Used for specific anemias, not for aldosteronism. Dose: Product-specific. Function: Stimulate red blood cell production. Mechanism: EPO receptor activation in marrow. Note: Off-topic for aldosteronism.
2) Growth hormone in deficiency (conceptual, 100 words)
For proven GH deficiency, not for aldosteronism. Dose: Individualized. Function: Tissue growth and metabolism. Mechanism: IGF-1 mediated anabolic effects. Note: Not used to treat aldosteronism.
3) Mesenchymal stem cell therapies (investigational, 100 words)
Explored for inflammatory and fibrotic diseases in trials. Dose: Protocol-based. Function: Immune modulation and tissue repair. Mechanism: Paracrine signals that reduce inflammation/fibrosis. Note: Not standard for aldosteronism.
4) Autologous stem cell mobilization (investigational, 100 words)
Used in hematologic settings, not endocrine hypertension. Dose: Protocol-specific. Function: Marrow rescue/regeneration. Mechanism: G-CSF mobilizes progenitors. Note: Not applicable to aldosteronism care.
5) Thymosin alpha-1 (investigational, 100 words)
Peptide with immune modulatory effects. Dose: Protocol-based. Function: Enhance T-cell function. Mechanism: Modulates innate/adaptive immunity. Note: Not a treatment for aldosteronism.
6) Bone-marrow–derived exosomes (experimental, 100 words)
Preclinical/regenerative applications. Dose: Research only. Function: Signal-mediated tissue effects. Mechanism: miRNA/protein cargo alters cell pathways. Note: Not used for aldosteronism.
Important: These regenerative/immune concepts do not treat aldosteronism. Effective medical therapy targets aldosterone (MR antagonists, ENaC blockers) and blood pressure.
Surgeries or procedures
1) Adrenal vein sampling (AVS)
Procedure: A specialist threads small catheters to both adrenal veins and samples blood to compare aldosterone on each side.
Why done: To determine if aldosterone is coming from one adrenal (unilateral adenoma) or both (bilateral hyperplasia). This guides therapy (surgery vs. medical).
2) Laparoscopic adrenalectomy (unilateral)
Procedure: Minimally invasive removal of one adrenal gland that has an aldosterone-producing adenoma.
Why done: If AVS confirms unilateral disease, surgery can cure or greatly improve aldosteronism and reduce BP medicines.
3) Laparoscopic adrenalectomy (bilateral—rare for BAH)
Procedure: Removal of both adrenals is not standard for bilateral hyperplasia because it causes lifelong adrenal insufficiency.
Why done: Considered only in exceptional, refractory cases with heavy specialist input.
4) Renal artery evaluation/intervention
Procedure: Imaging and, rarely, intervention when suspected renal artery stenosis contributes to RAAS activation.
Why done: To rule out secondary drivers of high aldosterone physiology when the story is unclear.
5) Catheter-based BP procedures (rare, investigational)
Procedure: Techniques like renal denervation are under study for resistant hypertension.
Why done: In selected resistant BP cases after optimal medical therapy, research approaches may be considered.
Preventions
Keep sodium intake low and steady every day.
Take medicines exactly as prescribed; do not stop suddenly.
Check blood pressure at home and keep a log.
Do regular lab tests for potassium and kidney function.
Maintain a healthy weight and stay physically active.
Limit alcohol and avoid tobacco/nicotine.
Sleep 7–9 hours and treat sleep apnea if present.
Manage stress with daily breathing or mindfulness.
See your clinician promptly for muscle weakness, cramps, or palpitations.
Educate family members about screening if they have early or resistant hypertension.
When to see doctors
See a clinician now if you have severe headache, chest pain, shortness of breath, fainting, or very high BP readings (for example, ≥180/120 mmHg). Arrange a visit soon if your home BP remains above your goal, if you have persistent muscle cramps or weakness, new palpitations, swelling in the legs, sudden weight gain from fluid, or medication side effects like breast tenderness, dizziness, or cough. Seek urgent care for severe low potassium symptoms such as paralysis or arrhythmia. See your doctor before starting any supplement, especially potassium, magnesium, or herbal products. Keep scheduled follow-ups for aldosterone-renin ratio checks, confirmatory testing, and imaging or adrenal vein sampling when recommended.
What to eat and what to avoid
Eat more of:
Fresh vegetables (leafy greens, tomatoes, peppers).
Fresh fruits (bananas, oranges, berries) if potassium is appropriate for you.
Beans, lentils, and unsalted nuts/seeds.
Whole grains (oats, brown rice, whole-wheat).
Lean proteins (fish, poultry, tofu), low-fat dairy.
Avoid or limit:
- Added salt and salty seasonings; taste food first.
- Processed meats, instant noodles, chips, and fast food.
- Canned soups and sauces unless labeled low sodium.
- Sugary drinks and heavy alcohol intake.
- Licorice (including some herbal teas/candies) because glycyrrhizin can mimic mineralocorticoid effects.
Frequently Asked Questions
1) Is aldosteronism with adrenal hyperplasia the same as regular hypertension?
No. It is a hormone-driven high blood pressure. The adrenal glands make too much aldosterone, which raises BP and lowers potassium. Treating aldosterone directly improves outcomes.
2) Can I have aldosteronism with normal potassium?
Yes. Many people have normal potassium but still have excess aldosterone. Screening is based on aldosterone-renin ratio, not potassium alone.
3) Why is bilateral hyperplasia different from an adrenal tumor?
A tumor (adenoma) is on one side and may be cured by surgery. Bilateral hyperplasia involves both glands, so treatment is usually medicines that block aldosterone.
4) Will I need medicines for life?
Many people with bilateral hyperplasia take long-term MR antagonists and other BP medicines. Consistent therapy protects the heart and kidneys.
5) How soon will treatment lower my blood pressure?
Some improvement occurs within days to weeks, but full benefit may take longer and often needs dose adjustments and lifestyle changes.
6) Can I take potassium supplements?
Only if your clinician says it is safe. With MR antagonists, potassium may rise, so supplements can be risky. Food-based potassium is often preferred, with labs checked.
7) What tests confirm the diagnosis?
Screening is the aldosterone-renin ratio, followed by confirmatory tests such as saline infusion, oral salt loading, or captopril challenge. Imaging and adrenal vein sampling help define the source.
8) Do I still need BP medicines if I feel fine?
Yes. Aldosteronism can silently damage the heart, kidneys, and brain. Medicines and lifestyle changes reduce long-term risks even when you feel well.
9) Will a low-salt diet really help?
Yes. Lower sodium reduces fluid retention and pressure, making your medicines work better and reducing aldosterone’s harm.
10) Can exercise replace medicine?
Exercise is very helpful but does not replace aldosterone-blocking therapy in bilateral hyperplasia. It works together with medicines.
11) Are MR antagonists safe?
They are widely used and effective. The main risk is high potassium, especially with kidney disease or certain drugs. Regular lab checks keep you safe.
12) What if I cannot tolerate spironolactone?
Eplerenone is more selective and often better tolerated. Amiloride is another option. Your clinician will choose based on your labs and medical history.
13) Could licorice raise my blood pressure?
Yes. Black licorice contains glycyrrhizin, which can mimic mineralocorticoid effects and raise BP. Avoid it unless your clinician clears a specific product.
14) Can this condition cause heart rhythm problems?
Yes. Low potassium and high aldosterone increase arrhythmia risk. Treating the condition and keeping potassium normal lowers that risk.
15) Will treating aldosteronism help protect my kidneys?
Yes. Effective treatment reduces protein in the urine and slows kidney damage over time.
Disclaimer: Each person’s journey is unique, treatment plan, life style, food habit, hormonal condition, immune system, chronic disease condition, geological location, weather and previous medical history is also unique. So always seek the best advice from a qualified medical professional or health care provider before trying any treatments to ensure to find out the best plan for you. This guide is for general information and educational purposes only. Regular check-ups and awareness can help to manage and prevent complications associated with these diseases conditions. If you or someone are suffering from this disease condition bookmark this website or share with someone who might find it useful! Boost your knowledge and stay ahead in your health journey. We always try to ensure that the content is regularly updated to reflect the latest medical research and treatment options. Thank you for giving your valuable time to read the article.
The article is written by Team RxHarun and reviewed by the Rx Editorial Board Members
Last Updated: October 19, 2025.
