Indian journal of pharmacologyNov 2, 2026

Severe low blood sodium linked to tirzepatide with signs of inappropriate antidiuretic hormone release

GLP-1 Therapies Weekly Brief ↗PubMed ↗DOI ↗OA ↗

Updated Nov 3, 2026

Abstract

Serum sodium in a patient on tirzepatide therapy dropped to 104 mmol/L, indicating severe symptomatic hyponatremia.

The patient experienced symptoms such as anorexia, weakness, and drowsiness 10 days after starting tirzepatide.
Biochemical analysis showed features compatible with the syndrome of inappropriate antidiuretic hormone secretion.
Despite normal renal, hepatic, hematologic, and acid-base parameters, the patient presented with a calculated serum osmolality of 224 mOsm/kg.
Urinary sodium levels remained elevated even after discontinuing diuretic therapy.
Management involved fluid restriction and hypertonic saline, leading to a progressive correction of sodium levels and improvement in clinical condition.
There may be an association between tirzepatide therapy and the development of severe euvolemic hyponatremia.

Simplified

Tirzepatide is a dual glucose-dependent insulinotropic polypeptide and glucagon-like peptide-1 receptor agonist that is being increasingly used for the management of type 2 diabetes mellitus and obesity. Gastrointestinal adverse effects associated with incretin-based therapies can influence water balance through nonosmotic vasopressin release and reduced oral solute intake. In this case report, we report a patient who developed severe symptomatic hyponatremia with biochemical features compatible with the syndrome of inappropriate antidiuretic hormone secretion temporally associated with tirzepatide therapy. A woman with type 2 diabetes mellitus and morbid obesity on regular insulin and chronic torsemide therapy presented with anorexia, weakness, and drowsiness 10 days after tirzepatide administration. Serum sodium was 104 mmol/L, and she was clinically euvolemic. Renal, hepatic, hematologic, acid-base, and other endocrine parameters were normal. The calculated serum osmolality was 224 mOsm/kg. Urinary sodium remained elevated after withdrawal of the diuretic. The patient was managed with fluid restriction and hypertonic saline, and this resulted in progressive correction of sodium and clinical improvement. This case suggests a potential association between tirzepatide therapy and severe euvolemic hyponatremia. Clinicians should consider electrolyte monitoring in patients receiving incretin-based therapy who develop significant gastrointestinal symptoms or reduced oral intake.

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Severe low blood sodium linked to tirzepatide with signs of inappropriate antidiuretic hormone release

Abstract

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