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Abstract: PO1117

Posaconazole-Related Mineralocorticoid Excess in a Patient with Acute Myeloid Leukemia

Session Information

Category: Fluid, Electrolyte, and Acid-Base Disorders

  • 902 Fluid, Electrolyte, and Acid-Base Disorders: Clinical


  • Mukku, Venkata Kishore R., The University of Texas Medical Branch at Galveston, Galveston, Texas, United States
  • Polani, Adnann Salim, Baylor College of Medicine, Houston, Texas, United States
  • Parvathareddy, Vishnupriyadevi, Baylor College of Medicine, Houston, Texas, United States
  • Mandayam, Sreedhar A., The University of Texas MD Anderson Cancer Center, Houston, Texas, United States

Posaconazole is an antifungal used for treatment and prophylaxis of invasive fungal infections in cancer patients. We report a case of posaconazole related mineralocorticoid excess in a patient with acute myeloid leukemia (AML).

Case Description

Patient is a 40-year-old male with past medical history of relapsed AML status post stem cell transplant, was admitted on 08/16/2020 to UTMDACC for pain, nausea, vomiting, diarrhea, and fatigue. He developed multiple complications streptococcus viridans bacteremia, candidemia, Graft Versus Host Disease, disseminated adenovirus, fungal pneumonia on posaconazole, tracheostomy due to severe mucositis with HSV-1 on Foscarnet. Nephrology was consulted for hypernatremia, hypokalemia and alkalosis. No nausea, vomiting, diarrhea was reported. Due to a combination of hypertension, metabolic alkalosis, hypokalemia and being on Posaconazole, we suspected Pseudo-hyperaldosteronism. Renin, aldosterone levels were checked which are low. CT scan of abdomen/pelvis did not show any adrenal tumors. Fractional excretion of potassium was high suggestive of renal loss. High 24-hour urine cortisol/cortisone ratio suggestive of mineralocorticoid excess. Posaconazole was changed to Voriconazole on 10/28/20. Due to persistent hypertension, spironolactone was increased and due to hypokalemia, amiloride was added. Twelve days after stopping Posaconazole all electrolyte and acid base abnormalities are resolved.


Combination of hypokalemia, hypertension and metabolic alkalosis need to suspect mineralocorticoid excess. Posaconazole inhibits 11 beta-hydroxysteroid dehydrogenase2 which prevents conversion of cortisol to cortisone. High cortisol than aldosterone leads to amplification of mineralocorticoid receptor action causing increase in activity, number of epithelial sodium channels (ENaC), Na-K-ATPase channels. Excess uptake of sodium leads to hypertension and creates increased negativity causing K+ and H+ losses leading to hypokalemia and alkalosis. Patients with mineralocorticoid excess can be treated with aldosterone receptor antagonist or ENaC blockers or by stopping or decreasing the dose of Posaconazole. Patients on posaconazole need to be monitored for hypokalemia, hypertension and alkalosis. However, not every patient will develop these which may be likely due to genetic predisposition.