Hyperaldosteronism (Conn's Syndrome)
Comprehensive integrative medicine approach for lasting healing and complete recovery
Understanding Hyperaldosteronism (Conn's Syndrome)
Hyperaldosteronism (Conn's Syndrome when caused by an adrenal adenoma) is a hormonal disorder where your adrenal glands produce too much aldosterone, causing your body to retain sodium and lose potassium. This results in treatment-resistant high blood pressure, low potassium levels, muscle weakness, and frequent urination. Primary hyperaldosteronism accounts for 5-10% of all hypertension cases and significantly increases cardiovascular risk even when blood pressure appears controlled.
Recognizing Hyperaldosteronism (Conn's Syndrome)
Common symptoms and warning signs to look for
High blood pressure that remains elevated despite taking 3 or more medications
Low potassium levels requiring prescription supplements (hypokalemia)
Frequent nighttime urination disrupting your sleep
Unexplained muscle weakness, cramps, or fatigue especially in legs
Persistent headaches, often severe and unresponsive to standard treatment
What a Healthy System Looks Like
In a healthy individual, the renin-angiotensin-aldosterone system (RAAS) maintains precise electrolyte and fluid balance. The adrenal cortex's zona glomerulosa produces aldosterone in response to angiotensin II, potassium levels, and ACTH. Aldosterone binds to mineralocorticoid receptors in the kidney's distal convoluted tubule and collecting duct, promoting sodium reabsorption and potassium excretion. This creates a negative feedback loop: when blood pressure rises, the juxtaglomerular apparatus reduces renin secretion, decreasing angiotensin II and aldosterone production. Normal aldosterone levels range from 2-9 ng/dL when upright, with renin activity of 0.65-5.0 ng/mL/hour, maintaining a normal aldosterone-to-renin ratio (ARR) below 20 ng/dL per ng/mL/hour.
How the Condition Develops
Understanding the biological mechanisms
Primary hyperaldosteronism develops through distinct mechanisms: (1) Aldosterone-producing adenoma (APA) - a benign tumor in the adrenal cortex autonomously secretes aldosterone independent of normal regulatory controls, accounting for 30-40% of cases. (2) Bilateral adrenal hyperplasia (BAH/idiopathic hyperaldosteronism) - diffuse enlargement of both adrenal glands with zona glomerulosa hyperplasia, representing 60-70% of cases. (3) Unilateral adrenal hyperplasia - rare unilateral gland enlargement. (4) Familial hyperaldosteronism - genetic mutations (FH-I/glucocorticoid-remediable aldosteronism, FH-II, FH-III, FH-IV) affecting aldosterone synthesis regulation. (5) Aldosterone-producing carcinoma - rare malignant tumors. The excess aldosterone causes sodium retention (expanding plasma volume), potassium wasting (hypokalemia), metabolic alkalosis, and direct cardiovascular toxicity independent of blood pressure effects. Chronically elevated aldosterone promotes cardiac fibrosis, vascular remodeling, endothelial dysfunction, and nephrosclerosis through mineralocorticoid receptor activation and oxidative stress pathways.
Key Laboratory Markers
Important values for diagnosis and monitoring
| Test | Normal Range | Optimal | Significance |
|---|---|---|---|
| Plasma Aldosterone Concentration (PAC) | 2-9 ng/dL (upright), 3-16 ng/dL (supine) | 2-6 ng/dL | Elevated in primary hyperaldosteronism; suppressed in secondary forms; measure in morning after 2 hours upright |
| Plasma Renin Activity (PRA) | 0.65-5.0 ng/mL/hour | 1.0-3.0 ng/mL/hour | Suppressed (<0.65) in primary hyperaldosteronism due to negative feedback; elevated in secondary causes |
| Aldosterone-to-Renin Ratio (ARR) | <20 ng/dL per ng/mL/hour | <10 ng/dL per ng/mL/hour | Screening test for primary hyperaldosteronism; >20 suggests PA; >30 with PAC >15 ng/dL highly suggestive |
| Serum Potassium | 3.5-5.0 mEq/L | 4.0-4.5 mEq/L | Hypokalemia (<3.5) present in 70-90% of cases; normokalemic PA increasingly recognized |
| 24-Hour Urinary Aldosterone | 2-20 mcg/24 hours (on normal sodium intake) | <14 mcg/24 hours | Confirmatory test; elevated despite high sodium intake (>200 mEq/day) confirms autonomous secretion |
| Serum Sodium | 135-145 mEq/L | 138-142 mEq/L | Often normal or mildly elevated due to water retention accompanying sodium retention |
| Serum Bicarbonate (CO2) | 22-29 mEq/L | 24-26 mEq/L | Metabolic alkalosis common (>29 mEq/L) due to hydrogen ion exchange for sodium in kidney |
| Plasma Metanephrines | <0.5 nmol/L (metanephrine), <0.9 nmol/L (normetanephrine) | Negative | Rules out pheochromocytoma which can mimic hyperaldosteronism symptoms |
| Adrenal CT/MRI | Normal adrenal glands <10 mm thick | No masses or nodules | Identifies adenomas (>10 mm suggests APA), hyperplasia, or incidentalomas; guides treatment decisions |
| Adrenal Vein Sampling (AVS) | Bilateral aldosterone similar | Lateralization ratio <2:1 | Gold standard for lateralization; cortisol-corrected aldosterone ratio >2:1 suggests unilateral disease |
Root Causes We Address
The underlying factors contributing to your condition
{"cause":"Aldosterone-Producing Adenoma (APA)","contribution":"30-40% of primary hyperaldosteronism cases","assessment":"Adrenal imaging showing unilateral nodule >10mm; lateralization on adrenal vein sampling; often younger age, more severe hypertension and hypokalemia"}
{"cause":"Bilateral Adrenal Hyperplasia (BAH/Idiopathic Hyperaldosteronism)","contribution":"60-70% of primary hyperaldosteronism cases","assessment":"Bilateral enlargement on imaging; no lateralization on AVS; older age, less severe presentation, often normokalemic"}
{"cause":"Familial Hyperaldosteronism Type I (FH-I/Glucocorticoid-Remediable Aldosteronism)","contribution":"<1% of cases; autosomal dominant","assessment":"Genetic testing for CYP11B1/CYP11B2 chimeric gene; early onset hypertension, often with family history; dexamethasone suppression test positive"}
{"cause":"Familial Hyperaldosteronism Type II","contribution":"Rare; autosomal dominant","assessment":"Genetic testing; CLCN2 chloride channel mutations; variable presentation with APA or BAH"}
{"cause":"Familial Hyperaldosteronism Type III","contribution":"Very rare","assessment":"KCNJ5 potassium channel mutations; severe early-onset hypertension, often with massive adrenal hyperplasia"}
{"cause":"Familial Hyperaldosteronism Type IV","contribution":"Rare","assessment":"CACNA1H calcium channel mutations; early onset hypertension"}
{"cause":"Unilateral Adrenal Hyperplasia","contribution":"1-2% of cases","assessment":"Unilateral uptake on AVS but no distinct adenoma on imaging; surgical cure possible"}
{"cause":"Aldosterone-Producing Carcinoma","contribution":"<1% of cases","assessment":"Large adrenal mass (>40mm), often with hormonal excess of other steroids; metastases may be present"}
{"cause":"Ectopic Aldosterone Production","contribution":"Extremely rare","assessment":"Ovarian or testicular tumors producing aldosterone; elevated aldosterone after adrenalectomy"}
Risks of Inaction
What happens if left untreated
{"complication":"Cardiovascular Disease","timeline":"Progressive over 5-15 years","impact":"4x increased risk of stroke, 2.5x increased risk of myocardial infarction, 2x increased risk of atrial fibrillation; aldosterone causes direct cardiac toxicity independent of blood pressure"}
{"complication":"End-Stage Renal Disease","timeline":"10-20 years of uncontrolled disease","impact":"Accelerated decline in kidney function due to glomerular hyperfiltration, proteinuria, and tubulointerstitial fibrosis; may require dialysis or transplant"}
{"complication":"Left Ventricular Hypertrophy and Heart Failure","timeline":"5-10 years","impact":"Aldosterone-mediated cardiac fibrosis leads to diastolic dysfunction, heart failure with preserved ejection fraction, and eventually systolic failure"}
{"complication":"Atrial Fibrillation","timeline":"Variable; risk increases with duration","impact":"12-fold increased risk compared to essential hypertension; aldosterone causes atrial electrical and structural remodeling"}
{"complication":"Cerebrovascular Events","timeline":"Progressive risk","impact":"Increased stroke risk from both hypertension and direct vascular effects of aldosterone on cerebral vessels"}
{"complication":"Osteoporosis and Fractures","timeline":"Chronic","impact":"Metabolic alkalosis and chronic potassium depletion increase bone turnover; vertebral and hip fracture risk increased"}
{"complication":"Pregnancy Complications","timeline":"If present during pregnancy","impact":"Increased risk of pre-eclampsia, placental abruption, intrauterine growth restriction, and preterm delivery"}
{"complication":"Quality of Life Impairment","timeline":"Chronic","impact":"Persistent fatigue, muscle weakness, nocturia disrupting sleep, medication side effects, and cardiovascular anxiety significantly reduce daily functioning"}
How We Diagnose
Comprehensive assessment methods we use
{"test":"Aldosterone-to-Renin Ratio (ARR) Screening","purpose":"Initial screening test for primary hyperaldosteronism","whatItShows":"Elevated aldosterone with suppressed renin suggests autonomous production; ARR >20 with PAC >15 ng/dL is positive screen"}
{"test":"Confirmatory Testing (Saline Infusion or Captopril Challenge)","purpose":"Confirm autonomous aldosterone secretion","whatItShows":"Failure to suppress aldosterone with volume expansion or ACE inhibition confirms primary hyperaldosteronism"}
{"test":"Adrenal CT or MRI","purpose":"Anatomical localization and characterization","whatItShows":"Identifies adenomas (>10mm), bilateral hyperplasia, or incidentalomas; guides further testing and treatment decisions"}
{"test":"Adrenal Vein Sampling (AVS)","purpose":"Lateralization to determine unilateral vs bilateral disease","whatItShows":"Cortisol-corrected aldosterone ratio between sides; >2:1 suggests unilateral disease amenable to surgery"}
{"test":"Comprehensive Metabolic Panel","purpose":"Assess electrolytes and kidney function","whatItShows":"Hypokalemia, metabolic alkalosis, mild hypernatremia, creatinine elevation suggesting renal involvement"}
{"test":"Genetic Testing","purpose":"Identify familial forms of hyperaldosteronism","whatItShows":"Mutations in CYP11B1/B2 (FH-I), CLCN2 (FH-II), KCNJ5 (FH-III), CACNA1H (FH-IV); guides family screening"}
{"test":"24-Hour Urinary Aldosterone","purpose":"Confirmatory test under controlled conditions","whatItShows":"Elevated aldosterone excretion despite high sodium intake (>200 mEq/day) confirms autonomous secretion"}
{"test":"Plasma Metanephrines","purpose":"Rule out pheochromocytoma","whatItShows":"Normal levels exclude pheochromocytoma which can present with similar symptoms"}
{"test":"Echocardiogram","purpose":"Assess cardiac target organ damage","whatItShows":"Left ventricular hypertrophy, diastolic dysfunction, or early heart failure changes"}
{"test":"Sleep Study (Polysomnography)","purpose":"Assess for obstructive sleep apnea","whatItShows":"Apnea-hypopnea index; strong association with hyperaldosteronism requiring concurrent treatment"}
Our Treatment Approach
How we help you overcome Hyperaldosteronism (Conn's Syndrome)
Phase 1: Diagnosis Confirmation and Initial Stabilization (Weeks 1-4)
{"phase":"Phase 1: Diagnosis Confirmation and Initial Stabilization (Weeks 1-4)","focus":"Confirm diagnosis, correct severe hypokalemia, initiate blood pressure control","interventions":"Complete biochemical screening (ARR, confirmatory testing). Correct hypokalemia with potassium supplementation and dietary counseling. Initiate mineralocorticoid receptor antagonist (spironolactone 25-50mg daily or eplerenone 50mg daily). Optimize other antihypertensives (ACE inhibitors, ARBs, calcium channel blockers). Screen for sleep apnea. Baseline echocardiogram and renal function assessment.\n"}
Phase 2: Subtype Classification and Treatment Planning (Weeks 4-12)
{"phase":"Phase 2: Subtype Classification and Treatment Planning (Weeks 4-12)","focus":"Determine unilateral vs bilateral disease; plan definitive therapy","interventions":"Adrenal imaging (CT/MRI) to identify adenomas. Adrenal vein sampling (AVS) for lateralization if surgery considered. Genetic testing if familial form suspected or early onset. Titration of mineralocorticoid antagonists to maximum tolerated dose (spironolactone up to 400mg/day). Monitor potassium and renal function closely. For unilateral disease: refer to endocrine surgeon for laparoscopic adrenalectomy.\n"}
Phase 3: Definitive Treatment (Months 3-6)
{"phase":"Phase 3: Definitive Treatment (Months 3-6)","focus":"Surgical cure for unilateral disease or optimal medical management for bilateral disease","interventions":"For unilateral disease: Laparoscopic adrenalectomy (posterior retroperitoneal or transperitoneal approach). Preoperative optimization of potassium and blood pressure. Postoperative monitoring for hypoaldosteronism (transient). For bilateral disease: Continue medical therapy with mineralocorticoid antagonists. Consider amiloride or triamterene if intolerant to spironolactone/eplerenone. Address cardiovascular risk factors aggressively.\n"}
Phase 4: Long-Term Management and Monitoring (Month 6+)
{"phase":"Phase 4: Long-Term Management and Monitoring (Month 6+)","focus":"Sustain remission, prevent cardiovascular complications, optimize quality of life","interventions":"Post-surgical patients: Monitor for recurrence (annual ARR), adrenal insufficiency if bilateral disease treated. Medical therapy patients: Regular monitoring of potassium, creatinine, blood pressure. Annual echocardiogram to assess cardiac remodeling reversal. Screen for metabolic syndrome components. Treat sleep apnea if present. Lifestyle optimization: sodium restriction, weight management, exercise. Consider glucocorticoid therapy for FH-I.\n"}
Diet & Lifestyle
Recommendations for optimal recovery
Lifestyle Modifications
Blood pressure monitoring: Home BP monitoring twice daily; proper technique essential, Weight management: Achieve and maintain healthy BMI; weight loss reduces aldosterone and blood pressure, Regular exercise: 150 minutes moderate aerobic activity weekly; improves insulin sensitivity and cardiovascular health, Sleep apnea treatment: CPAP or oral appliance if diagnosed; significantly improves aldosterone and blood pressure, Stress management: Chronic stress activates RAAS; meditation, yoga, breathing exercises, Smoking cessation: Essential for cardiovascular risk reduction, Limit NSAIDs: Can worsen kidney function and blood pressure control, Regular sleep schedule: 7-9 hours nightly; poor sleep activates sympathetic nervous system, Avoid excessive heat: Heat can worsen hypotension if over-medicated
Recovery Timeline
What to expect on your healing journey
Phase 1 (Weeks 1-4): Diagnosis confirmation and initial stabilization. ARR screening and confirmatory testing completed. Hypokalemia corrected. Mineralocorticoid receptor antagonist initiated. Blood pressure begins improving.
Phase 2 (Weeks 4-12): Subtype classification. Adrenal imaging and adrenal vein sampling performed. Genetic testing if indicated. Medication titration to optimal doses. Cardiovascular risk assessment completed.
Phase 3 (Months 3-6): Definitive treatment. For unilateral disease: laparoscopic adrenalectomy performed. For bilateral disease: optimal medical therapy established. Sleep apnea treatment initiated if present.
Phase 4 (Month 6+): Long-term management. Post-surgical patients monitored for recurrence and adrenal function. Medical therapy patients maintained on mineralocorticoid antagonists. Regular monitoring of potassium, kidney function, blood pressure, and cardiac status. Lifestyle optimization continues.
Surgical Recovery: Hospital stay 1-3 days. Return to normal activities 2-4 weeks. Blood pressure often normalizes within days to weeks post-surgery. Full metabolic recovery by 3 months.
Note: Individual timelines vary based on severity, presence of complications, surgical candidacy, and response to treatment. Lifelong monitoring is required even after successful surgery due to risk of recurrence or contralateral disease.
How We Measure Success
Outcomes that matter
Blood pressure <130/80 mmHg on minimal or no medications (post-surgical)
Blood pressure controlled on tolerated medical regimen (bilateral disease)
Serum potassium maintained between 4.0-4.5 mEq/L without supplementation
Aldosterone-to-renin ratio normalized or significantly improved
Reduction or elimination of antihypertensive medications
Resolution of hypokalemia-related symptoms (muscle weakness, cramps, fatigue)
Reduction in nocturia frequency
Regression of left ventricular hypertrophy on echocardiogram
Stable or improved kidney function (creatinine, eGFR)
Resolution of metabolic alkalosis
Improved sleep quality (if sleep apnea treated concurrently)
Improved exercise tolerance and energy levels
Reduction in cardiovascular risk markers (lipids, inflammatory markers)
Quality of life improvement: reduced headaches, better concentration, less fatigue
Frequently Asked Questions
Common questions from patients
What is the difference between Conn's Syndrome and hyperaldosteronism?
Conn's Syndrome specifically refers to primary hyperaldosteronism caused by an aldosterone-producing adrenal adenoma (APA), named after Dr. Jerome Conn who first described it in 1955. Hyperaldosteronism is the broader term encompassing all causes of excess aldosterone production, including bilateral adrenal hyperplasia (the most common cause), familial forms, and rare adrenal cancers. All Conn's Syndrome is hyperaldosteronism, but not all hyperaldosteronism is Conn's Syndrome.
Why is my blood pressure so difficult to control with medications?
Primary hyperaldosteronism causes treatment-resistant hypertension because the excess aldosterone promotes sodium retention, volume expansion, and increased peripheral vascular resistance through mechanisms that standard antihypertensives (ACE inhibitors, ARBs, calcium channel blockers, beta-blockers) don't fully address. Mineralocorticoid receptor antagonists (spironolactone, eplerenone) specifically block aldosterone's effects and are essential for blood pressure control in this condition. Many patients require 3-4 medications for adequate control.
Will I need surgery, or can this be treated with medication?
Treatment depends on the underlying cause. If adrenal vein sampling (AVS) shows unilateral disease (adrenal adenoma or unilateral hyperplasia), laparoscopic adrenalectomy offers a potential cure in 30-60% of cases, with significant improvement in most others. If bilateral adrenal hyperplasia is diagnosed, lifelong medical management with mineralocorticoid receptor antagonists is typically required. Surgery is usually recommended for younger patients (<40), those with hypokalemia, and clear unilateral adenomas on imaging.
Can primary hyperaldosteronism be cured?
If caused by a unilateral aldosterone-producing adenoma (APA) and treated with adrenalectomy, 30-60% of patients achieve complete cure (normal blood pressure without medications), while another 30-40% show significant improvement requiring fewer medications. However, if bilateral adrenal hyperplasia (BAH) is the cause, medical management is required long-term. Early diagnosis and treatment offer the best chances for cure or significant improvement.
Why do I have to get up multiple times at night to urinate?
Nocturia (frequent nighttime urination) occurs in hyperaldosteronism because the kidneys lose concentrating ability due to chronic hypokalemia and tubular damage. Additionally, when you lie down at night, the excess fluid that accumulated in your legs during the day (dependent edema) returns to circulation, increasing kidney filtration. This phenomenon, called nocturnal polyuria, is a hallmark symptom of hyperaldosteronism and often improves with treatment.
Is this condition hereditary? Should my family members be tested?
Most cases (95%+) are sporadic, but 5% represent familial hyperaldosteronism with genetic inheritance. If you were diagnosed before age 20, have a family history of early-onset hypertension or stroke, or have bilateral disease with specific features, genetic testing is recommended. If a familial form is identified, first-degree relatives should be screened with blood pressure monitoring and ARR testing, particularly before age 20.
Medical References
- 1.Funder JW, Carey RM, Mantero F, et al. The Management of Primary Aldosteronism: Case Detection, Diagnosis, and Treatment: An Endocrine Society Clinical Practice Guideline. J Clin Endocrinol Metab. 2016;101(5):1889-1916. PMID: 26934393 - Comprehensive clinical practice guidelines for diagnosis and management.
- 2.Rossi GP, Bernini G, Caliumi C, et al. A prospective study of the prevalence of primary aldosteronism in 1,125 hypertensive patients. J Am Coll Cardiol. 2006;48(11):2293-2300. PMID: 17161262 - Key prevalence study establishing 5-10% of hypertension cases.
- 3.Monticone S, D'Ascenzo F, Moretti C, et al. Cardiovascular events and target organ damage in primary aldosteronism compared with essential hypertension: a systematic review and meta-analysis. Lancet Diabetes Endocrinol. 2018;6(1):41-50. PMID: 28886928 - Demonstrates increased cardiovascular risk independent of blood pressure.
- 4.Hundemer GL, Curhan GC, Yozamp N, Wang M, Vaidya A. Cardiometabolic outcomes and mortality in medically treated primary aldosteronism: a retrospective cohort study. Lancet Diabetes Endocrinol. 2018;6(1):51-59. PMID: 28886929 - Long-term outcomes comparing medical vs surgical management.
- 5.Williams TA, Lenders JWM, Mulatero P, et al. Outcomes after adrenalectomy for unilateral primary aldosteronism: an international consensus on outcome measures and analysis of remission rates in an international cohort. Lancet Diabetes Endocrinol. 2017;5(9):689-699. PMID: 28576687 - International consensus on surgical outcomes and remission criteria.
- 6.Stowasser M, Gordon RD, Gunasekera TG, et al. High rate of detection of primary aldosteronism, including surgically treatable forms, after 'non-selective' screening of hypertensive patients. J Hypertens. 2003;21(11):2149-2157. PMID: 14597846 - Evidence supporting broader screening criteria.
- 7.Calhoun DA, Nishizaka MK, Zaman MA, Thakkar RB, Weissmann P. Hyperaldosteronism among black and white subjects with resistant hypertension. Hypertension. 2003;41(4):892-896. PMID: 12623974 - Prevalence in resistant hypertension populations.
- 8.Conn JW, Louis LH. Primary aldosteronism: a new clinical entity. Trans Assoc Am Physicians. 1955;68:215-231. PMID: 13299331 - Original description of Conn's Syndrome.
- 9.Mulatero P, Monticone S, Bertello C, et al. Long-term cardio- and cerebrovascular events in patients with primary aldosteronism. J Clin Endocrinol Metab. 2013;98(12):4826-4833. PMID: 24108065 - Long-term cardiovascular outcomes data.
- 10.Satoh F, Morimoto R, Ono Y, et al. Measurement of peripheral plasma 18-oxocortisol can discriminate unilateral adenoma from bilateral diseases in primary aldosteronism. Hypertension. 2015;65(5):1096-1102. PMID: 25753906 - Novel biomarker for subtype differentiation.
Ready to Start Your Healing Journey?
Our integrative medicine experts are ready to help you overcome Hyperaldosteronism (Conn's Syndrome).