Abstract

Chloride was recently recognized to play an important role in the pathophysiology of heart failure (HF). Chloride manipulation, including the use of acetazolamide, may be a requisite therapeutic target in HF treatment. An 87-year-old male patient with advanced HF and hypertrophic cardiomyopathy was admitted to the hospital due to hypochloremia (94mEq/L) and hyponatremia (134mEq/L) under diuretic treatment with azosemide, spironolactone, and tolvaptan. On admission, HF-related signs of overhydration were lacking, but B-type natriuretic peptide was moderately elevated. The etiology of the hypochloremia/natremia state was depletion of both electrolytes based on serum analysis and spot urinary concentrations. Immediately after admission, acetazolamide (500mg/d) was prescribed to correct the hypochloremia in parallel with cessation of the preceding administration of azosemide and spironolactone, and tapering off of the tolvaptan over 7 days. Under treatment, both serum chloride and sodium concentrations recovered to normal (108mEq/L and 148mEq/L, respectively), and the serum potassium concentration decreased from 3.9mEq/L to 2.4mEq/L. Urinary concentrations of sodium and potassium increased from 18mEq/L to 31mEq/L and from 19mEq/L to 51.5mEq/L respectively, in concordance with the changes in serum concentrations, but the chloride concentration decreased from 18mEq/L to 12mEq/L, opposite the changes in the serum concentration.<Learning objective: The present case confirms that the classic drug acetazolamide, although rarely used now for HF treatment, is a potent “chloride-regaining” or “chloride-retaining diuretic” with concomitant activity to reduce serum potassium. Additionally, this case study highlights the importance of monitoring both serum and urinary electrolyte concentrations to determine the electrolyte disturbance and efficacy of diuretic treatment through analytic evaluation of changes in the serum electrolytes and their tubular reabsorption in the kidney.>

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