Abstract: FR-PO0893
Refractory Hyperkalemia in a Patient with Iatrogenic Adrenal Insufficiency
Session Information
- Fluid, Electrolyte, and Acid-Base Disorders: Case Reports - 1
October 23, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Fluid, Electrolytes, and Acid-Base Disorders
- 1102 Fluid, Electrolyte, and Acid-Base Disorders: Clinical
Authors
- Malla, Sajit, Tulane University School of Medicine, New Orleans, Louisiana, United States
- Pittappilly, Matthew, Tulane University School of Medicine, New Orleans, Louisiana, United States
- Alvarado, Flor, Tulane University School of Medicine, New Orleans, Louisiana, United States
Introduction
Severe refractory hyperkalemia in the setting of preserved kidney function should prompt evaluation for adrenal insufficiency. We present a case of life-threatening, refractory hyperkalemia caused by the synergistic suppressive effects of megestrol acetate, fluconazole, and enoxaparin on the adrenal hormone synthesis.
Case Description
A 54-year-old male with a history of HIV on antiretroviral therapy, poorly controlled diabetes mellitus, cryptococcal meningitis on fluconazole maintenance was admitted to the hospital for multiple issues. The hospital course was protracted and the patient had been on PO fluconazole, PO TMP-SMX, SC enoxaparin along with PO megestrol for 7 days before being discontinued. During the course of his hospital stay, he was found to have refractory hyperkalemia (7.6 mmol/L). He also had an emergency hemodialysis for his severe hyperkalemia. With valid prerequisites including adequate distal nephron sodium delivery (urine sodium 127 mEq/L) and urine osmolarity > plasma osmolarity the TTKG was calculated to be 1. Earlier in his hospital course, adrenal function was found to be adequate. Later in the hospital course, as a part of workup for hyperkalemia, he was found to have findings of low AM cortisol (0.4 μg/dL) with low DHEAS, low serum aldosterone (<1 ng/dL) with normal plasma renin activity (1.945 ng/mL/hr) and low ACTH (3.1 pg/mL). A high-dose ACTH stimulation test was consistent with adrenal insufficiency. Initiation of fludrocortisone and hydrocortisone promptly resolved his hyperkalemia.
Discussion
Albeit with its many limitations, in this context a very low TTKG in the setting of severe hyperkalemia, suggested inappropriately low renal potassium secretion due to low serum aldosterone.
The profound hyperkalemia resulted from a synergistic "multi-hit" mechanism where megestrol-induced central HPA axis suppression along with enoxaparin and fluconazole-mediated inhibition of steroid hormone synthesis, lead to combined deficiency of cortisol and aldosterone that was acutely exacerbated by the abrupt withdrawal of megestrol. His poorly controlled diabetes mellitus also likely contributed to his hyperkalemia via non aldosterone mediated mechanism.
Nephrologists must maintain a high index of suspicion for iatrogenic adrenal insufficiency when multiple steroid-modulating medications are used, especially following the withdrawal of such agents.