Abstract: PO1468
Posaconazole-Induced Hypokalemia in a Hemodialysis Patient
Session Information
- Fluid, Electrolyte, and Acid-Base Disorders: Clinical - 1
October 22, 2020 | Location: On-Demand
Abstract Time: 10:00 AM - 12:00 PM
Category: Trainee Case Report
- 902 Fluid, Electrolyte, and Acid-Base Disorders: Clinical
Authors
- Patel, Mital, Ronald Reagan UCLA Medical Center, Los Angeles, California, United States
- Nguyen, Minhtri K., Ronald Reagan UCLA Medical Center, Los Angeles, California, United States
Introduction
Posaconazole is a commonly used antifungal agent that is used for prophylaxis in many transplant recipients. Its side effect profile can vary from cardiovascular effects to metabolic derangements, such as hypokalemia. A prior case report of apparent mineralocorticoid excess (AME) secondary to Posaconazole therapy has been reported in 2017; however, this has not previously been reported in the ESRD patient population.
Case Description
A 68-year-old male with past medical history of idiopathic pulmonary fibrosis who underwent left lung transplant in December 2019 was consulted for acute kidney injury (AKI). Etiology of AKI was attributed to Tacrolimus induced thrombotic microangiopathy that ultimately required initiation of hemodialysis. Posaconazole 200mg PO daily was used for anti-fungal prophylaxis. Throughout the hospitalization, persistent hypokalemia was observed despite dialyzing the patient against a 4K bath. Further hypokalemia evaluation revealed plasma renin level at lower limit of normal (0.5ng/mL/hr), and low plasma aldosterone level at <3.0 ng/dL. 24 hr urinary cortisol-to-cortisone ratio was non-diagnostic likely due to an inadequate collection (creatinine 160 mg/24 hr).
Discussion
We identified a case that mimics apparent mineralocorticoid excess syndrome, where patients receiving Posaconazole behave as if they have increased serum aldosterone levels; however, when serum levels are measured, aldosterone levels are in fact low. Patients are unable to metabolize cortisol to cortisone due to a defect in 11β-hydroxysteroid dehydrogenase. This leads to an accumulation of cortisol, allowing it to bind to the aldosterone receptor and increase sodium entry intracellularly via the epithelial sodium channel (ENaC). Stimulation of the ENaC then leads to potassium secretion and subsequent hypokalemia. Common lab findings include: hypokalemia, low serum renin and aldosterone levels, and elevated urine cortisol/cortisone ratio. Similar presentations can be seen with licorice ingestion, hereditary AME, and carbenoxolone use.
This case illustrates the unique presentation of Posaconazole-induced hypokalemia in an ESRD patient (a population that typically experiences hyperkalemia and poor clearance of potassium), who was dialyzed against a 4K bath but persistently remained hypokalemic.