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Hyperaldosteronism

Hyperaldosteronism is defined as the increased secretion of aldosterone from the zona glomerulosa of the adrenal cortex. Hyperaldosteronism may be primary (resulting from autonomous secretion), or secondary (resulting from physiological secretion due to stimulation of the RAAS). Classically, hyperaldosteronism presents with hypertension, hypokalemia, and metabolic alkalosis, although recent studies have suggested that hypokalemia is less common than originally thought in primary hyperaldosteronism. Patients with hypertension who are treatment resistant and/or associated with hypokalemia should be screened for hyperaldosteronism by determining their plasma aldosterone concentration and plasma renin activity. Confirmatory tests and an abdominal CT scan are required to conclusively diagnose primary hyperaldosteronism. Management involves the use of aldosterone receptor antagonists and surgical excision of any aldosterone-secreting tumors.

Last updated: July 20, 2025 235 views

Definition: Primary hyperaldosteronism is characterized by autonomous overproduction of aldosterone from the zona glomerulosa of the adrenal cortex, independent of the renin-angiotensin-aldosterone system (RAAS).

  • Primary hyperaldosteronism: autonomous (renin-independent) secretion of aldosterone
  • Secondary hyperaldosteronism: physiological oversecretion of aldosterone that occurs in response to overstimulation of the RAAS, triggered by decreases in renal blood flow.

Key Concept
  • Primary = Problem with adrenal: "Adrenal won't listen to signals"
  • Secondary = Problem elsewhere: "Adrenal responding normally to abnormal signals"
  • Diagnostic key: Renin levels distinguish between the two
 ملاحظة

Etiology of Hyperaldosteronism
Type Etiology Clinical Features
Primary hyperaldosteronism
  • Bilateral idiopathic hyperplasia → most common (∼60%)
  • Adrenal adenoma (Conn syndrome) → 35%
  • Adrenal carcinoma
  • Familial hyperaldosteronism
  • No edema (aldosterone escape)
  • Resistant hypertension
  • Hypokalemia (may be mild)
  • Suppressed renin
Secondary hyperaldosteronism
  • Heart failure
  • Cirrhosis with ascites
  • Renal artery stenosis
  • Chronic kidney disease
  • Renin-producing tumors
  • Edema present
  • Volume depletion
  • Elevated renin
  • Underlying disease evident

Overview: The Role of Aldosterone

Aldosterone is a mineralocorticoid hormone that serves as the body's primary regulator of sodium and water balance. Its fundamental purpose is to increase blood pressure through three key mechanisms:

  • ↑ Sodium reabsorption → ↑ Water retention → ↑ Blood volume
  • ↑ Potassium excretion
  • ↑ Hydrogen ion excretion

 

Normal Physiology: The RAAS Cascade

Step 1: Initiation

The renin-angiotensin-aldosterone system (RAAS) activates when the body senses:

  • ↓ Blood pressure or ↓ Effective blood volume
  • ↓ Sodium delivery to the distal tubule
  • ↑ Sympathetic nervous system activity

 

Step 2: The Cascade

  1. Juxtaglomerular cells (kidney) → Release RENIN
  2. Renin converts Angiotensinogen (liver) → Angiotensin I
  3. ACE (lungs) converts Angiotensin I → ANGIOTENSIN II
  4. Angiotensin II stimulates Zona Glomerulosa → ALDOSTERONE

 

Step 3: Direct Aldosterone Stimulation

Two primary stimuli directly trigger aldosterone release:

  • Angiotensin II (via RAAS)
  • Hyperkalemia (direct effect on zona glomerulosa)

 

Net Effects of Aldosterone Action

Parameter Effect Mechanism
Blood Pressure ↑↑ Volume expansion from Na+/H2O retention
Serum Na+ ↑ Enhanced renal reabsorption
Serum K+ ↓ Increased renal excretion
Serum pH ↑ H+ excretion (metabolic alkalosis)

 

Pathophysiology of Hyperaldosteronism

Primary Hyperaldosteronism: Autonomous Secretion

  • Key Concept: The adrenal gland produces aldosterone independently of physiologic stimuli
  • Sequence of Events:
    1. Autonomous aldosterone production (adenoma or hyperplasia)
    2. Excessive Na+ and water retention → Hypertension
    3. Negative feedback suppresses renin → ↓ PRA (key diagnostic feature)
    4. Continued K+ and H+ excretion → Hypokalemia and alkalosis
  • The Aldosterone Escape Phenomenon
    Despite continuous aldosterone excess, patients with primary hyperaldosteronism do NOT develop edema:
  • Initial Na+ retention → ↑ Blood volume
  • Volume expansion triggers compensatory mechanisms:
    • ↑ Atrial natriuretic peptide (ANP) release
    • ↑ Pressure natriuresis
    • ↓ Proximal tubule Na+ reabsorption
  • Result: New steady state without edema

     

    Secondary Hyperaldosteronism: Physiologic Response

    • ↓ Renal blood flow due to other diseases
    • Key Concept: The RAAS is physiologically activated due to decreased renal perfusion
    • Common Triggers:
      • Heart failure → ↓ Cardiac output
      • Cirrhosis → ↓ Effective blood volume
      • Renal artery stenosis → ↓ Renal perfusion
    • Sequence of Events:
      1. ↓ Renal perfusion sensed by JG cells
      2. ↑ Renin release → ↑ Angiotensin II → ↑ Aldosterone
      3. Persistent volume depletion despite Na+ retention
      4. NO aldosterone escape → Progressive edema ★

     

    Key Pathophysiologic Differences
    Feature Primary Secondary
    Initiating event Autonomous aldosterone ↓ Renal perfusion
    Renin levels Suppressed (↓) ★ Elevated (↑) ★
    Volume status Euvolemic / mild expansion Volume depleted
    Edema Absent (escape present) Present (no escape)
    Pathophysiology Inappropriate secretion Physiologic response

     

       

    Pathophysiology Pearls
    • Aldosterone escape: Why primary hyperaldosteronism patients don't get edema
    • Renin suppression: Key diagnostic feature in primary disease
    • K+ wasting: Can be severe, especially with diuretic use
    • No escape in secondary: Underlying disease prevents compensation
    		 ملاحظة

    Due to the effects of aldosterone, clinical presentation includes:

    • Hypertension, often resistant to treatment.
    • Hypokalemia:  Serum potassium may be normal at baseline, but severe hypokalemia can be triggered by diuretic therapy.
    • Mild hypernatremia may be present.
    • Metabolic alkalosis.

    Peripheral edema may be mild or absent due to aldosterone escape (increased intravascular volume increases pressure natriuresis and atrial natriuretic peptide release, thereby limiting net sodium retention)

    Clinical Pearls
    • "Hypertension without edema": Think primary hyperaldosteronism
    • "Resistant hypertension + normal K+": Still screen for hyperaldosteronism
    • "Diuretic-induced severe hypokalemia": Red flag for underlying hyperaldosteronism
    • "Young hypertensive patient": Consider secondary causes including hyperaldosteronism
    		 ملاحظة

    • Elevated plasma aldosterone concentration (PAC) and suppressed plasma renin activity (PRA); PAC/PRA ratio >20
      • In contrast, elevated PAC and PRA with a PAC/PRA ratio ~10 suggests secondary hyperaldosteronism (eg, renovascular hypertension, cirrhosis, renin-secreting tumor)
    • Confirmatory tests (eg, saline infusion test, oral sodium loading test [showing absence of aldosterone suppression due to renin-independent aldosterone secretion])
    • Adrenal imaging (CT or MRI) to identify adenoma or hyperplasia

     

    • Adenoma:  Surgical resection (adrenalectomy)
    • Bilateral adrenal hyperplasia:  Mineralocorticoid receptor antagonists (eg, spironolactone, eplerenone)

    Mnemonic for Primary vs Secondary Hyperaldosteronism

    RENIN Mnemonic for Differentiation

    • R: Renin LOW = Primary hyperaldosteronism
    • E: Edema ABSENT = Primary hyperaldosteronism
    • N: No underlying disease = Primary hyperaldosteronism
    • I: Independent aldosterone secretion = Primary
    • N: Normal heart/kidneys = Primary hyperaldosteronism
    		 جملة تذكرية
    Mnemonic for Aldosterone Effects

    SIMON Mnemonic for Aldosterone Actions

    • S: Sodium retention
    • I: Increases blood pressure
    • M: Mineralocorticoid receptor activation
    • O: Opposes potassium (causes K+ loss)
    • N: Nephron collecting duct target
    		 جملة تذكرية
    Mnemonic for Diagnostic Workup

    PACS Mnemonic for Diagnosis

    • P: PAC/PRA ratio >20 (screening)
    • A: Aldosterone suppression test (confirmation)
    • C: CT/MRI adrenal imaging (localization)
    • S: Sampling of adrenal veins (lateralization)
    		 جملة تذكرية
    Mnemonic for Clinical Presentation

    HYPER Mnemonic for Hyperaldosteronism

    • H: Hypertension (resistant)
    • Y: Young patient with severe HTN
    • P: Potassium low (hypokalemia)
    • E: Edema absent (aldosterone escape)
    • R: Renin suppressed (in primary)
    		 جملة تذكرية
    Mnemonic for Treatment Options

    AMES Mnemonic for Management

    • A: Adenoma = Adrenalectomy (surgery)
    • M: Multiple/bilateral = Medical therapy
    • E: Eplerenone or spironolactone (MR antagonists)
    • S: Surgery cure rate 30-60% for HTN
    		 جملة تذكرية