Kidney Week

Abstract: FR-PO0885

A Case of Postadrenalectomy Hyponatremia in Primary Hyperaldosteronism: Unmasking Hidden Sodium Dysregulation

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

• Aguirre, Eloise A., AtlantiCare Regional Medical Center Atlantic City Campus, Atlantic City, New Jersey, United States

Eloise A. Aguirre, MD

• Grewal, Mehtab, AtlantiCare Regional Medical Center Atlantic City Campus, Atlantic City, New Jersey, United States

Mehtab Grewal, MD

• Aguirre, Zedrick, AtlantiCare Regional Medical Center Atlantic City Campus, Atlantic City, New Jersey, United States

Zedrick Aguirre, MD

• Thakkar, Priyesh T., AtlantiCare Regional Medical Center Atlantic City Campus, Atlantic City, New Jersey, United States

Priyesh T. Thakkar, DO, MBA, FASN

Introduction

Primary hyperaldosteronism due to unilateral adrenal adenoma is best managed by adrenalectomy. Post-resection hyperkalemia is a common complication thus potassium levels are monitored after surgery. We present a case of a patient with severe hyponatremia after a unilateral adrenalectomy for primary hyperaldosteronism.

Case Description

This is a case of a 62-year-old male with a 20-year history of treatment-resistant hypertension who underwent right unilateral adrenalectomy with pathology confirming an aldosterone secreting adrenal cortical adenoma. On postoperative day 11, he presents with generalized weakness and subsequently admitted for severe hyponatremia of 118 mmol/L with urine indices concerning for SIADH thus managed as such with sodium chloride tablets, fluid restriction, and tolvaptan, ultimately improving sodium levels to 133 mmol/L prior to discharge. He was readmitted on postoperative day 22 for severe hyponatremia at 111 mmol/L. Despite fluid restriction and increase of sodium chloride tablets, no improvement was noted. Repeat urine indices were not consistent with SIADH. Hormone levels revealed normal TSH, cortisol, ACTH, and renin levels, but low aldosterone level, consistent with isolated mineralocorticoid deficiency. Based on this assumption, he was trialed on fludrocortisone 0.1 mg OD, later increased to TID with eventual normalization of sodium.

Discussion

Most patients have good clinical outcomes after surgery with normalization of the plasma aldosterone levels. This is an interesting case because post adrenalectomy patients typically present with hyperkalemia and recovery of RAAS. His persistent hyponatremia may be related to non-recovery of his aldosterone producing cells. These cells are normally stimulated by angiotensin II thus long-term suppression may cause atrophy of the zona glomerulosa. In extreme cases with complete loss of aldosterone, the kidney loses its sodium retaining capacity leading to massive urine sodium losses and activating the ADH-thirst feedback mechanism, worsening the dilution of the plasma sodium. His hyponatremia resolving after fludrocortisone confirmed that aldosterone deficiency was the underlying cause. Although hyperkalemia is a common complication post adrenalectomy, isolated hyponatremia is an uncommon complication post adrenalectomy that similarly responds with mineralocorticoid supplementation.