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: SA-PO719

Pressor Dose Vasopressin-Induced Acute Hyponatremia

Session Information

Category: Fluid, Electrolytes, and Acid-Base Disorders

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

Authors

  • Nassar, Raed, Montefiore Health System, Bronx, New York, United States
  • Brogan, Maureen, Montefiore Health System, Bronx, New York, United States
  • Gupta, Sonali, Montefiore Health System, Bronx, New York, United States
  • Alzyood, Laith, Montefiore Health System, Bronx, New York, United States
  • Lee, Roy, Montefiore Health System, Bronx, New York, United States
Introduction

Vasopressin infusion is commonly used in intensive care unit for circulatory shock but has rarely been associated with hyponatremia. We describe a case of severe hyponatremia in a patient receiving vasopressin infusion that improved upon discontinuation.

Case Description

A 54-year-old, 74-kilogram male, with a history of interstitial lung disease, was admitted to the intensive care unit for acute hypoxic respiratory failure and shock due to COVID-19 pneumonia. A vasopressin infusion, at 0.03 units/minute, was initiated as an adjunctive medication to Norepinephrine. The patient’s sodium level decreased from 136 mEq/L to 122 mEq/L over the first 15 hours. Urine output over this time was 1.2 Liters. Once vasopressin was discontinued, the urine output increased to 300 mL/hour with an osmolarity of less than 100 mOsm/kg. The serum sodium rapidly normalized to 135 mEq/L in 9 hours. The patient required desmopressin and a five percent dextrose infusion for treatment of overcorrection of hyponatremia.

Discussion

Vasopressin, at doses of 0.03 units/minute, is a common medication given in the intensive care unit to support circulatory collapse. Vasopressin can exert antidiuretic effects through interaction with V2 receptors in the renal collecting duct cells by incorporation of aquaporin 2 channels allowing passive free water reabsorption across an osmotic gradient. This results in water intoxication with subsequent hyponatremia. In our patient, discontinuation of Vasopressin resulted in a prompt diuresis and correction of hyponatremia.