What is the role of sodium sulfate and furosemide tests in the workup of hyperchloremic acidosis?

Updated: Oct 18, 2018
  • Author: Sai-Ching Jim Yeung, MD, PhD, FACP; Chief Editor: Romesh Khardori, MD, PhD, FACP  more...
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In healthy individuals, administering a sodium salt of a nonreabsorbable anion in the presence of a sodium-avid state results in negative intratubular potential and thus in increased proton and potassium secretion. In patients with either secretory or voltage defects, the urine will not become maximally acidic.

The test is performed by restricting salt to less than 1 g/d Na+ for 3 days and orally administering 1 mg of fludrocortisone in the evening, 12 hours before the sodium sulfate infusion, in order to ensure a sodium-avid state. The following morning, 500 mL of 4% sodium sulfate is administered intravenously over 1 hour. Urine pH, potassium excretion, and net acid excretion should be obtained.

A normal response does not necessarily rule out an acidification defect, because a normal response can be observed in patients with hyperkalemic dRTA and in those with reversible voltage-dependent defects, as with lithium.

False-positive results can occur when the infusion is too rapid or when sodium avidity is absent because inadequate preparation or aldosterone resistance causes a bicarbonate-losing osmotic diuresis, thus raising the urine pH.

Because sodium sulfate is not commercially available, this method is largely limited to research settings. A more practical method involves orally administering 1 mg fludrocortisone the evening before testing and then giving 1 mg/kg of oral or intravenous furosemide the following morning. Evidence suggests that furosemide enhances distal acidification by increasing distal sodium delivery, and results should be interpreted in the same manner as for the sodium sulfate test.

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