Kidney Week

Abstract: FR-PO0883

Fire and Drought: Anti-N-Methyl-D-Aspartate (NMDA) Receptor Encephalitis Presenting with 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

• Sakhuja, Priyal, Icahn School of Medicine at Mount Sinai, New York, New York, United States

Priyal Sakhuja, DO

• Rao, Kishan, Icahn School of Medicine at Mount Sinai, New York, New York, United States

Kishan Rao, MD

• Menon, Aiswarya, Icahn School of Medicine at Mount Sinai, New York, New York, United States

Aiswarya Menon, MBBS, MD

• Rein, Joshua L., Icahn School of Medicine at Mount Sinai, New York, New York, United States

Joshua L. Rein, DO, FASN

• Uribarri, Jaime, Icahn School of Medicine at Mount Sinai, New York, New York, United States

Jaime Uribarri, MD

• Farouk, Samira S., Icahn School of Medicine at Mount Sinai, New York, New York, United States

Samira S. Farouk, MD, MS, FASN

Introduction

Anti-NMDAR encephalitis involves IgG autoantibodies targeting GluN1, causing receptor internalization and reduced NMDA signaling. NMDA receptors are present in hypothalamic pathways involved in AVP production and thirst regulation and in the kidney, where they contribute to vascular hemodynamic regulation and tubular transport. We present a case of hypernatremia in a kidney transplant patient where NMDAR-mediated inflammation likely contributed to dysregulation of thirst and AVP production while also impairing renal concentrating capacity.

Case Description

A 36-year-old male with ESKD post-kidney transplant and NMDAR encephalitis (treated with IVIG and rituximab) presented to the clinic with hypernatremia of 162 and AKI on allograft CKD. He denied any decrease in oral intake of water and was fatigued but not altered. Chart review revealed multiple prior admissions for hypernatremia attributed to poor oral intake; however, the urine osmolarity was variable (179 mOsm/kg up to as high as 400-600 mOsm/kg). DDAVP was initiated with some improvement in urine osmolarity but persistent hypernatremia.

Discussion

This case demonstrates the complications of hypernatremia in patients with anti-NMDA encephalitis. Increased osmolality normally causes urine concentration >600 mOsm/kg, stimulating AVP secretion. If urine osmolality remains low, it indicates AVP deficiency or resistance. The variation of urine osmolality and response to desmopressin indicated partial central diabetes insipidus. Diagnosis was delayed due to fluctuating mental status and initial perception of decreased free water intake as cause of hypernatremia. Dehydration alone does not explain uniformly low urine osmolality in hypernatremia. Complexity was heightened by transplant status, since allograft denervation and aquaporin-2 and NKCC2 channel downregulation may impair urine-concentrating ability. Antibody-mediated NMDAR internalization, established in cortical neurons, may similarly affect GluN1-expressing hypothalamic nuclei and circumventricular organs, impairing osmoregulation. In anti-NMDAR encephalitis, low urine osmolality with hypernatremia should prompt CDI evaluation rather than assuming decreased intake alone. Renal transplant recipients may have intrinsic concentrating deficits due to denervation and ischemia-reperfusion injury, which must be considered when interpreting urine osmolality for CDI diagnosis.