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Difficulty: HardNephrology

Match each patient's clinical presentation and laboratory profile with the most likely underlying renal mechanism responsible for the derangements.

  • A 55-year-old treated for essential hypertension has asymptomatic laboratory findings of K+K^+ 2.8 mEq/L, HCO3−HCO_3^- 32 mEq/L, and a 24-hour urine calcium of 75 mg.Inhibition of the Na+Na^+-Cl−Cl^- cotransporter in the distal convoluted tubule
  • A 60-year-old treated for decompensated heart failure develops leg cramps; labs show K+K^+ 3.0 mEq/L, HCO3−HCO_3^- 31 mEq/L, and a 24-hour urine calcium of 350 mg.Inhibition of the Na+Na^+-K+K^+-2Cl−2Cl^- cotransporter in the thick ascending limb
  • A 45-year-old with a psychiatric history complains of profound thirst; labs show Na+Na^+ 149 mEq/L, serum osmolality 312 mOsm/kg, and urine osmolality 140 mOsm/kg despite water deprivation.Downregulation of aquaporin-2 channels in the principal cells of the collecting duct
  • A 35-year-old receiving intravenous therapy for cryptococcal meningitis develops Na+Na^+ 139 mEq/L, K+K^+ 2.7 mEq/L, HCO3−HCO_3^- 14 mEq/L, Cl−Cl^- 113 mEq/L, and a urine pH of 6.5.Formation of pores in the distal tubular membrane leading to increased proton permeability

Answer

Each clinical presentation connects to a distinct pharmacological etiology. The hypocalciuric patient matches the distal convoluted tubule mechanism (thiazide). The hypercalciuric patient matches the thick ascending limb mechanism (loop diuretic). The patient with dilute polyuria matches collecting duct resistance (lithium). The patient with normal anion gap metabolic acidosis and high urine pH matches distal tubule proton back-leak (Amphotericin B).
The matching requires connecting classic laboratory derangements to the specific site and mechanism of action of drugs in the nephron, utilizing distinguishing features like urine calcium levels, osmolality, and acid-base status.

Step-by-Step Solution

1
Analyze the first patient's profile to identify the responsible mechanism.
The profile shows hypokalemic metabolic alkalosis with hypocalciuria (75 mg/day). This matches the mechanism of thiazide diuretics.
Thiazides inhibit the Na+Na^+-Cl−Cl^- cotransporter in the distal convoluted tubule, uniquely enhancing distal calcium reabsorption unlike other diuretics.
2
Analyze the second patient's profile to identify the responsible mechanism.
The profile shows hypokalemic metabolic alkalosis with hypercalciuria (350 mg/day). This matches the mechanism of loop diuretics.
Loop diuretics inhibit the Na+Na^+-K+K^+-2Cl−2Cl^- cotransporter in the thick ascending limb, blocking paracellular calcium reabsorption.
3
Analyze the third patient's profile to identify the responsible mechanism.
The profile shows hypernatremia with inappropriately dilute urine despite water deprivation. This indicates nephrogenic diabetes insipidus, typically caused by lithium.
Lithium downregulates aquaporin-2 channels in the collecting duct, causing resistance to antidiuretic hormone.
4
Analyze the fourth patient's profile to identify the responsible mechanism.
The profile shows a non-anion gap metabolic acidosis (AG = 12) with hypokalemia and elevated urine pH (6.5), diagnostic of a Type 1 (distal) renal tubular acidosis caused by Amphotericin B.
Amphotericin B creates pores in the distal tubular membrane, leading to proton back-leak and failure to acidify the urine appropriately.

Key Concept

Specific pharmacological agents produce distinct renal syndromes based on their molecular mechanisms: thiazides cause hypocalciuria, loop diuretics cause hypercalciuria, lithium causes nephrogenic diabetes insipidus, and Amphotericin B causes Type 1 renal tubular acidosis.
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Topics

Nephrology

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