Kidney Week

Abstract: FR-PO0604

Rare Link Between Hyponatremia and Neurologic Symptoms: Acute Hepatic Porphyria

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

• Burgos Martinez, Lidynell M, Universidad de Puerto Rico, San Juan, San Juan, Puerto Rico

Lidynell M Burgos Martinez, MD

• Adams Chahin, Juan J., Universidad de Puerto Rico, San Juan, San Juan, Puerto Rico

Juan J. Adams Chahin, MD

• Vazquez-Fernandez, Paola M., Universidad de Puerto Rico, San Juan, San Juan, Puerto Rico

Paola M. Vazquez-Fernandez, MD

• Ocasio Melendez, Ileana E., Universidad de Puerto Rico, San Juan, San Juan, Puerto Rico

Ileana E. Ocasio Melendez, MD, FASN

Introduction

Hyponatremia is a common finding in acute hepatic porphyrias (AHPs), particularly during acute attacks. This is often due to the syndrome of inappropriate antidiuretic hormone secretion (SIADH), leading to water retention and dilution of sodium. This abstract details the management of hyponatremia in a 57-year-old male with AHP.

Case Description

A 56-year-old male patient with a medical history of Hypertension and chronic low back pain presented to the hospital due to progressive proximal upper and lower extremity weakness of 2 weeks of evolution. Neuroimaging, including brain and cervical MRI with and without gadolinium, was unremarkable, and no intracranial abnormalities were observed. Initial laboratories showed a CBC within normal limits, and chemistry was remarkable for mild hyponatremia with adequate renal parameters.
The patient was managed with IVIG and steroids, with poor clinical improvement. Further work-up results, including markedly elevated urine porphyrins, were consistent with AHP. On day 28, the patient was treated with carbohydrate loading with D10% IV infusion for 48 hours and subsequently developed altered mental status, associated with acute worsening hyponatremia. He was managed with 3% saline infusion and fluid restriction. The hyponatremia work-up was consistent with SIADH. The patient was started on Hemin, and further management was established by the hematology-oncology service.

Discussion

This case illustrates the importance of considering AHP in patients presenting with unexplained hyponatremia and progressive neurologic symptoms. The development of SIADH and worsening hyponatremia following carbohydrate loading highlights the metabolic complexity of AHP. Clinical management should include monitoring of electrolytes and cautious correction of hyponatremia. Early recognition and collaborative care are critical for managing complex cases of hyponatremia and improving patient outcomes.

Laboratory results

Digital Object Identifier (DOI)

• doi: 10.1681/ASN.20258848j49q