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Bartter, Liddle, and Conn Syndromes


Bartter, Liddle, and Conn Syndromes

A practical comparison of salt-handling disorders causing metabolic alkalosis

Disorders of renal sodium handling are frequently tested and clinically relevant because they present with characteristic patterns of blood pressure, electrolytes, and hormonal changes. Bartter syndrome, Liddle syndrome, and Conn syndrome all cause metabolic alkalosis but differ fundamentally in their mechanisms and clinical profiles.

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Bartter Syndrome

Salt-wasting disorder mimicking chronic loop diuretic use


Bartter syndrome is a hereditary defect of ion transport in the thick ascending limb of the loop of Henle, most commonly involving the Na–K–2Cl cotransporter (NKCC2) or related channels.


Pathophysiology


Impaired sodium reabsorption in the loop of Henle


Renal sodium loss → extracellular volume depletion


Secondary activation of RAAS


Increased distal sodium delivery → potassium and hydrogen ion loss



Key Biochemical Changes


Increased


Renin


Aldosterone



Decreased


Sodium


Blood volume


Potassium



Clinical Features


Normal or low blood pressure (no hypertension despite high aldosterone)


Polyuria, polydipsia


Growth retardation (pediatric cases)


Metabolic alkalosis



Core Concept


> High renin, high aldosterone, no hypertension





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Liddle Syndrome


Pseudohyperaldosteronism


Liddle syndrome is a rare genetic disorder caused by constitutive activation of the epithelial sodium channel (ENaC) in the collecting duct.


Pathophysiology


Excessive sodium reabsorption independent of aldosterone


Volume expansion → suppression of RAAS


Increased potassium and hydrogen ion secretion



Key Biochemical Changes


Increased


Sodium


Blood volume


Blood pressure



Decreased


Renin


Aldosterone


Potassium



Clinical Features


Early-onset hypertension


Hypokalemia


Metabolic alkalosis


Poor response to spironolactone



Treatment Principle


ENaC blockers: amiloride or triamterene



Core Concept


> Hypertension without aldosterone





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Conn Syndrome (Primary Hyperaldosteronism)


True aldosterone excess


Conn syndrome is caused by autonomous aldosterone secretion, usually from an adrenal adenoma or bilateral adrenal hyperplasia.


Pathophysiology


Excess aldosterone → increased sodium reabsorption


Volume expansion → suppressed renin


Increased potassium and hydrogen ion excretion



Key Biochemical Changes


Increased


Sodium


Blood volume


Blood pressure


Aldosterone



Decreased


Renin


Potassium



Clinical Features


Resistant hypertension


Hypokalemia (may be mild or absent)


Metabolic alkalosis



Diagnostic Clue


High aldosterone-to-renin ratio



Core Concept


> Hypertension due to high aldosterone





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Side-by-Side Summary


Feature Bartter Liddle Conn


Primary defect NKCC2 / loop transport ENaC overactivity Aldosterone excess

Blood pressure Normal / low High High

Renin ↑ ↓ ↓

Aldosterone ↑ ↓ ↑

Potassium ↓ ↓ ↓

Acid–base status Metabolic alkalosis Metabolic alkalosis Metabolic alkalosis

Key clue Salt wasting, no HTN HTN without aldosterone HTN with high aldosterone




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Exam Pearls


Bartter = diuretics effect + no hypertension


Liddle = low renin, low aldosterone, hypertension


Conn = low renin, high aldosterone, hypertension




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For more cardiology and medicine infographics, visit:

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