Abstract: FR-PO0615
AKI with Hyponatremia from Rivaroxaban-Induced Bilateral Adrenal Hemorrhage
Session Information
- Fluid, Electrolyte, and Acid-Base Disorders: Clinical - 2
November 07, 2025 | Location: Exhibit Hall, 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
- Jin, Alison, The University of Texas Southwestern Medical Center, Dallas, Texas, United States
- Kumar, Monika, The University of Texas Southwestern Medical Center, Dallas, Texas, United States
- Sims, Robert D, VA North Texas Health Care System, Dallas, Texas, United States
- Khayat, Maurice I., The University of Texas Southwestern Medical Center, Dallas, Texas, United States
Introduction
Adrenal hemorrhage is a rare but life-threatening complication often associated with autoimmune disease, trauma, or anticoagulant use. Laboratory evidence of adrenal insufficiency (AI) may include hyponatremia or acute kidney injury (AKI) from excessive natriuresis and ADH release. Given the variable, nonspecific presentation of these conditions (e.g., fatigue, nausea, anorexia, weight loss), a high index of suspicion is required to avoid a missed diagnosis.
Case Description
A 57-year-old male presented with fatigue, anorexia, weight loss (45 lb) and recurrent emesis. One month prior, he had been diagnosed with saddle pulmonary embolus (PE) requiring thrombectomy and was discharged on rivaroxaban. On presentation, vitals were within normal limits, but labs revealed AKI (creatinine 2.1 mg/dL with baseline 1.4 mg/dL) and hyponatremia (130 mEq/L), initially responsive to isotonic fluid but with unexplained recurrence.
During workup of his emesis, an abdominal MRI revealed possible bilateral adrenal hemorrhage. Concern was subsequently raised for AI. Morning cortisol was low at 3.0 ug/dL and remained 3.0 ug/dL at 30 and 60 minutes post-cosyntropin administration. Endocrinology was consulted and started stress dose IV hydrocortisone (HC) with taper to oral (20mg/10mg every morning/evening) and fludrocortisone 0.05 mg daily. The patient's symptoms resolved, and his renal function and plasma sodium both normalized.
After initial conversion from rivaroxaban to a heparin drip, hematology was consulted. Considering his recent PE, elevated risk for recurrent thrombosis, and hemodynamic stability the patient was maintained on anticoagulation with transition to low molecular weight heparin due to its shorter duration of action. He was monitored in the outpatient setting and successfully converted to apixaban after a period of clinical stability.
Discussion
The nonspecific presentation of AI can complicate accurate diagnosis. A high index of suspicion is required in patients with risk factors, especially in the absence of hypotension. As this case illustrates, adrenal hemorrhage is important to consider in patients on anticoagulation presenting with AI. Although rare, adrenal hemorrhage has been described with the newer direct oral anticoagulants. Early detection can facilitate timely treatment and earlier engagement of appropriate consultants to improve outcomes.