ASN's Mission

To create a world without kidney diseases, the ASN Alliance for Kidney Health elevates care by educating and informing, driving breakthroughs and innovation, and advocating for policies that create transformative changes in kidney medicine throughout the world.

learn more

Contact ASN

1401 H St, NW, Ste 900, Washington, DC 20005


The Latest on Twitter

Kidney Week

Abstract: FR-PO575

Supratherapeutic Posaconazole: An Emerging Cause of Apparent Mineralocorticoid Excess (AME)

Session Information

  • Trainee Case Reports - III
    October 26, 2018 | Location: Exhibit Hall, San Diego Convention Center
    Abstract Time: 10:00 AM - 12:00 PM

Category: Trainee Case Reports

  • 902 Fluid and Electrolytes: Clinical


  • Atsava-Svate, Narisorn, University of Colorado Denver, Denver, Colorado, United States
  • Jani, Alkesh, University of Denver Colorado, Aurora, Colorado, United States

Apparent mineralocorticoid excess (AME) causes severe hypertension accompanied by metabolic alkalosis with hypokalemia. Substances which are well known to cause AME include glycyrrhizic and glycyrrhetinic acid found in licorice. These compounds competitively inhibit the enzyme called 11 Beta Hydroxysteroid Dehydrogenase type 2 (11β- HSD2). Lack of 11β- HSD2 caused higher cortisol available to bind the mineralocorticoid receptor, and results in ENaC-mediated Na reabsorption.
Posaconazole, the broad-spectrum azole group antifungal agent, is commonly used for prophylaxis in patients with AML and severe neutropenia. Literature review revealed that posaconazole at supratherapeutic level can also inhibit 11β- HSD2 and cause apparent mineralocorticoid excess (AME).

Case Description

A 37 years old Caucasian female with refractory acute myelogenous leukemia (AML) with normal baseline blood pressure(100-120/65-80mmHg). She had neutropenia after third re-induction chemotherapy with G-CLAM regimen. She was then started on oral posaconazole 300 mg daily for fungal prophylaxis. One month later she then developed refractory hypokalemia with metabolic alkalosis and new onset hypertension (180/110mmHg). We were giving her potassium replacement 60-80 mEq/day, but her serum potassium level remained less than 3.3 mEq/L. Her serum cortisol level was 18.2 mcg/dL, plasma renin activity <0.167 ng/mL/h, plasma aldosterone level < 1ng/dL. Serum posaconazole level was 1800 ng/mL. Discontinuation of posaconazole, with documented normal therapeutic posacoanzole level, resulted in improvement of hypertension, refractory hypokalemia and metabolic alkalosis. All clinical features resolved within 2 weeks after discontinuation of posaconazole.


We suggest that posaconazole level should be part of laboratory investigations in patients who are treated with posaconazole and have new onset of hypertension, hypokalemia and metabolic alkalosis. Posaconazole, at supratherapeutic level, inhibits 11 Beta Hydroxysteroid Dehydrogenase type 2 and causes apparent mineralocorticoid excess (AME).