Kidney Week

Abstract: FR-PO0879

A Case of Hyponatremia Followed by Central Diabetes Insipidus

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

• Cancarevic, Ivan, Mass General Brigham Inc, Boston, Massachusetts, United States

Ivan Cancarevic, MD

• Yatim, Karim, Mass General Brigham Inc, Boston, Massachusetts, United States

Karim Yatim, MD

• Lundquist, Andrew L., Mass General Brigham Inc, Boston, Massachusetts, United States

Andrew L. Lundquist, MD, PhD

• Babitt, Jodie L., Mass General Brigham Inc, Boston, Massachusetts, United States

Jodie L. Babitt, MD

Introduction

Serum sodium levels are tightly regulated by Antidiuretic Hormone’s (ADH) effect on the kidney. Central diabetes insipidus (CDI) is characterized by decreased production or release of ADH, due to disorders of the hypothalamus or neurohypophysis. CDI can be secondary to trauma, autoimmune disease, malignancy, infections, etc. Patients present with aquaresis that, if not compensated for by increased free water intake, leads to hypernatremia. Low plasma copeptin levels in the setting of water deprivation and hypernatremia distinguish CDI from nephrogenic diabetes insipidus, which is due ADH resistance.

Case Description

We present a case of a 35-year-old male who presented after being found unconscious. Due to his respiratory status, he was intubated. He was found to have severe rhabdomyolysis with hypovolemic hyponatremia to 113 mEq/L, hypocalcemia, and metabolic acidosis. Urine Na was 21 mOsm/kg, and urine osmolality was 792 mOsm/kg. After resuscitation with isotonic fluids, serum sodium overcorrected to 122 mEq/L over 14 hours. Over the next 24 hours, patient became polyuric, making 5-7 L of urine per day, continuously overcorrecting sodium and requiring repeated use of ddAVP. Multiple attempts to wean ddAVP were unsuccessful. Over the following 2 days, patient’s sodium levels normalized, however, polyuria persisted even at the point when patient became hypernatremic to 148 mEq/L. At that time, with ddAVP held for 30 hours, the plasma copeptin level was checked and was undetectable with slight increase in urine osmolality consistent with the diagnosis of partial CDI (from between 100 and 250 mOsm/kg to between 500 and 700 mOsm/kg). Brain imaging was unremarkable, although pituitary imaging was notable for a 3x3 mm hypoenhancement, thought to be either artefact or microadenoma. Eventually, as patient improved, his polyuria resolved, ddAVP was discontinued and sodium normalized, suggesting a resolution of CDI.

Discussion

We hypothesize that cerebral edema caused by hyponatremia affected the neurons responsible for ADH synthesis and/or release leading to partial CDI with resolution over time. It is also possible that it was a separate process, such as edema of the non-functioning pituitary adenoma that compressed those neurons. This case underscores the importance of close monitoring of serum sodium levels and urine output even beyond the moment of correction, especially in cases of severe hyponatremia.