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Difficulty: HardNephrology

Match each clinical and laboratory profile of hypokalemic metabolic alkalosis to its most likely underlying etiology.

  • Hypertension, hypokalemia, metabolic alkalosis, low plasma renin activity, elevated serum aldosterone.Primary hyperaldosteronism
  • Normotension, hypokalemia, metabolic alkalosis, urine chloride < 10 mEq/L, signs of volume depletion.Surreptitious vomiting
  • Normotension, hypokalemia, metabolic alkalosis, urine chloride > 20 mEq/L, hypomagnesemia, hypocalciuria.Gitelman syndrome
  • Hypertension, hypokalemia, metabolic alkalosis, low plasma renin activity, low serum aldosterone.Liddle syndrome
  • Normotension, hypokalemia, metabolic alkalosis, urine chloride > 20 mEq/L, hypercalciuria, normal serum magnesium.Bartter syndrome

Answer

Primary hyperaldosteronism is characterized by hypertension and high aldosterone; Surreptitious vomiting presents with normotension and low urine chloride; Gitelman syndrome presents with normotension, high urine chloride, and hypocalciuria; Liddle syndrome presents with hypertension and low aldosterone; and Bartter syndrome presents with normotension, high urine chloride, and hypercalciuria.
The diagnostic algorithm for metabolic alkalosis requires synthesis of multiple variables. Volume-expanded states present with hypertension, and the aldosterone level distinguishes primary hyperaldosteronism (high) from Liddle syndrome (low). Volume-contracted (normotensive) states are distinguished by urine chloride: low urine chloride indicates extrarenal loss like vomiting, while high urine chloride indicates a renal tubular defect. Finally, tubular defects are differentiated by calcium excretion (hypercalciuria in Bartter vs. hypocalciuria in Gitelman).

Step-by-Step Solution

1
Evaluate blood pressure to categorize the etiologies of hypokalemic metabolic alkalosis into hypertensive and normotensive states.
Hypertensive conditions include Primary hyperaldosteronism and Liddle syndrome; normotensive conditions include Surreptitious vomiting, Gitelman syndrome, and Bartter syndrome.
Blood pressure serves as a surrogate for effective circulating volume, immediately dividing the differential diagnosis into volume-expanded versus volume-contracted etiologies.
2
For hypertensive profiles, assess the plasma renin activity and serum aldosterone levels.
Elevated aldosterone with suppressed renin points to Primary hyperaldosteronism. Suppressed aldosterone with suppressed renin points to Liddle syndrome.
Liddle syndrome is caused by an autonomous ENaC channel activation, which expands volume and suppresses both renin and aldosterone, distinguishing it from an aldosterone-producing adenoma.
3
For normotensive profiles, analyze the urine chloride concentration to determine saline responsiveness.
A urine chloride < 10 mEq/L indicates a saline-responsive state (e.g., vomiting). A urine chloride > 20 mEq/L indicates a saline-resistant tubular disorder.
In extrarenal chloride loss (vomiting), the kidneys appropriately conserve chloride. In intrinsic renal tubular wasting, the kidneys inappropriately excrete chloride despite volume depletion.
4
Differentiate the saline-resistant normotensive profiles using urine calcium and serum magnesium levels.
Hypocalciuria and hypomagnesemia identify Gitelman syndrome. Hypercalciuria identifies Bartter syndrome.
Gitelman syndrome shares the physiology of thiazide diuretics (DCT defect), while Bartter syndrome shares the physiology of loop diuretics (thick ascending limb defect).

Key Concept

Evaluation of metabolic alkalosis relies on sequentially analyzing blood pressure, urine chloride concentration, and the renin-aldosterone axis.
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Topics

Nephrology

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