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Abstract: SA-PO741

A Man with Serum [Na] 163 mM Who Is Not Thirsty

Session Information

Category: Fluid, Electrolytes, and Acid-Base Disorders

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

Authors

  • Orlev-Shitrit, Eithan, Maine Medical Center, Portland, Maine, United States
  • Segal, Alan, Maine Medical Center, Portland, Maine, United States

Group or Team Name

  • MMP Nephrology.
Introduction

Lack of thirst sensation is a rare cause of hypertonicity, as thirst is the main defense to maintain isotonicity and normal intracellular volume. Hypertonicity is sensed by osmoreceptor cells, which control thirst and ADH release. The ability to sense/act on thirst is both necessary and sufficient to prevent dehydration, with ADH playing a supportive role by increasing the kidney water absorbtion. We present a case of a patient who developed hypertonicity due to an acquired injury resulting in defects in both thirst (resulting in hypodipsia) and ADH release (resulting in reduced water retention).

Case Description

A 60-year-old man with a history of CHF, DM, HTN and CKD ([Cr] 1.5 mg/dL) was admitted for cardiogenic shock. He was managed with diuresis and discharged with Torsemide and water/salt restrictions. During the admission, [Na] increased from 132 to 154 mM. Four days after discharge, he was re-admitted when follow-up laboratory tests showing serum [Na] of 163 mM and urine osmolality of only 369 mOsm/L. Surprisingly, he did not complain of thirst. He was treated with D5W, reduced Torsemide dose, and daily water consumption of ~ 2.5 L. Within two days, serum [Na] corrected to 144 mM. CT head did not show a brain lesion (cardiac defibrillator precluded MRI). A transient resumption of Torsemide and liberation of water consumption led to an immediate worsening of hypernatremia. He was discharged with serum [Na] of 147 mM and instructions to keep strict water intake of ~3 L per day. To date, the patient is isotonic.

Discussion

Our patient developed severe hypernatremia, which—although initially promoted by water restriction and Torsemide—was maintained by a remarkable lack of thirst sensation and urine concentration defect. Most of the patients with this rare condition, are young and have an identified CNS etiology (e.g. tumor), whereas our patient was 60 years old without a brain lesion. We conclude that our patient developed hypertonicity due to a rare combination of lack of thirst (hypodipsia) and partial arginine vasopressin deficiency and was treated successfully with an increased water intake.