MON-873 - Adrenal Insufficiency Treatment in Patients without Kidneys: Bridging the Gap between Physiologic Rationale and Evidence-Based Practice

Adrenal insufficiency management relies on glucocorticoid and mineralocorticoid replacement to restore stress response, and cardiovascular regulation. Fludrocortisone acts primarily on distal renal tubules to enhance sodium reabsorption and potassium excretion, raising blood pressure through electrolyte mechanism. While extrarenal vascular effects have been proposed, including sensitization of smooth muscle to catecholamines, their clinical significance in anephric patients remains unclear. Current guidelines recommend fludrocortisone discontinuation in dialysis patients as it is no longer needed, yet no case reports, or protocols exist for this population.

A 23-year-old male with bilateral nephrectomy following abdominal gunshot wound at age 18, requiring hemodialysis (M/W/F), presented with weakness, dizziness, nausea, and vomiting. His chronic medications included prednisone 5 mg twice daily, fludrocortisone 0.1 mg twice daily, and midodrine 5 mg three times daily for refractory hypotension. Despite five years of medical management, he had never seen an endocrinologist and experienced recurrent emergency visits requiring ICU-level vasopressor support. Vital signs revealed severe hypotension (78/53 mmHg, MAP 61 mmHg), tachycardia (107 bpm), and hypoxemia (94% room air). Laboratory findings showed leukocytosis (14.5 K/μL), hypoglycemia (60 mg/dL), and hyperkalemia (6.6 mmol/L). Endocrinology consultation initiated stress-dose hydrocortisone 50 mg IV every 8 hours for suspected adrenal crisis precipitated by pneumonia. Recognizing the physiologic futility of mineralocorticoid therapy without kidneys, fludrocortisone was discontinued. By day 2, blood pressure stabilized (100/65 mmHg, MAP 76 mmHg), allowing glucocorticoid taper to prednisone 15 mg daily. Discharge recommendations emphasized permanent fludrocortisone discontinuation and endocrinology follow-up. Alarmingly, one month later, the patient was readmitted to another institution with identical hypotensive complaints, and fludrocortisone was restarted upon discharge, reflecting fundamental misunderstanding of its mechanism in anephric patients.

This highlight a critical knowledge gap, and bring the attention that no published literature addresses fludrocortisone use in anephric patients or optimal management strategies for AI. Fludrocortisone cannot function without kidneys. The medication's reinitiation at an outside institution exemplifies how lack of mechanistic understanding perpetuates inappropriate polypharmacy and delays effective therapy. Management should focus on optimizing glucocorticoid replacement and maximizing alternative vasopressor strategies, particularly midodrine dose escalation, as this population faces heightened vulnerability to intradialytic hypotension.

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