ASN's Mission

To create a world without kidney diseases, the ASN Alliance for Kidney Health elevates care by educating and informing, driving breakthroughs and innovation, and advocating for policies that create transformative changes in kidney medicine throughout the world.

learn more

Contact ASN

1401 H St, NW, Ste 900, Washington, DC 20005

email@asn-online.org

202-640-4660

The Latest on X

Kidney Week

Abstract: PUB090

Severe Hypernatremia from Central Diabetes Insipidus and Panhypopituitarism Due to Central Nervous System (CNS) Lymphoma in Advanced HIV

Session Information

Category: Fluid, Electrolytes, and Acid-Base Disorders

  • 1102 Fluid, Electrolyte, and Acid-Base Disorders: Clinical

Authors

  • Huerta, Carlos H., Methodist Dallas Medical Center, Dallas, Texas, United States
  • Bacani, Rigel, Methodist Dallas Medical Center, Dallas, Texas, United States
  • Singh, Adhish, Methodist Dallas Medical Center, Dallas, Texas, United States
  • Chowdhury, Renuka, Methodist Dallas Medical Center, Dallas, Texas, United States
Introduction

Severe hypernatremia in hospitalized patients is often attributed to dehydration, poor intake, or sepsis. New hypernatremia with marked polyuria developing later in admission should raise concern for central diabetes insipidus (CDI). Concurrent CDI and panhypopituitarism from hypothalamic-pituitary infiltration by lymphoma is uncommon. In HIV-associated diffuse large B-cell lymphoma (DLBCL), CNS involvement may occur through direct or secondary spread and present with CDI and severe hypernatremia.

Case Description

A 56-year-old man with advanced HIV infection (CD4 <50 cells/uL, off antiretroviral therapy) and nasopharyngeal DLBCL was admitted with septic shock from Pseudomonas aeruginosa bacteremia. His course was complicated by oliguric AKI requiring fluid resuscitation and vasopressors. Later in admission, he developed persistent polyuria >5 L/day and serum sodium increased to 165 mmol/L despite IV fluids, prompting evaluation for CDI. Brain MRI showed a 2.2 cm enhancing lesion involving the hypothalamus and optic chiasm extending from the nasopharyngeal mass (Figure 1), consistent with secondary CNS lymphoma. Labs showed low ACTH (3.7 pg/mL), low TSH (0.24 mIU/L), low free T4, low LH, and low testosterone, with mildly elevated prolactin (24.8 ng/mL), consistent with panhypopituitarism. Glucocorticoids were started before thyroid hormone replacement. Desmopressin and free water replacement were initiated; however, before meaningful correction of hypernatremia, the family chose comfort care given progressive neurologic decline.

Discussion

In prolonged hospitalizations complicated by sepsis and AKI, CDI from hypothalamic infiltration may develop gradually and go unrecognized until hypernatremia and polyuria become severe. When CDI occurs with multiple pituitary hormone deficiencies in an immunocompromised patient, malignant infiltration of the hypothalamic-pituitary axis should be strongly considered. Glucocorticoids must precede thyroid hormone replacement to avoid adrenal crisis.

Figure 1. Brain MRI demonstrating a 2.2 cm enhancing mass at the hypothalamus and optic chiasm (blue arrows) consistent with secondary CNS lymphoma.