C53-03 Transient Vasopressin Resistance During Acute Tubular Necrosis Recovery: A Reversible Cause of ICU-associated Hypernatremia

Abstract Introduction Transient arginine vasopressin resistance (AVP-R), a reversible form of nephrogenic diabetes insipidus, results from collecting-duct insensitivity to vasopressin and manifests as polyuria with hypernatremia. ICU-associated hypernatremia occurs in up to 10 % of critically ill patients, but AVP-R during renal tubular regeneration is rarely recognized. Prompt identification is crucial, as inappropriate desmopressin administration or overly rapid sodium correction can lead to neurologic injury and delay renal recovery. Case Presentation An 81-year-old woman with baseline stage 2 CKD was admitted to the ICU for severe community-acquired pneumonia complicated by two cardiac arrests and multiorgan failure. Baseline renal function was normal but deteriorated to KDIGO stage 3 AKI. Urine indices were consistent with intrinsic renal injury from ischemic ATN. During the oliguric phase, urine output was 0.5 mL/kg/hr; with renal recovery, she developed polyuria 7 L/day and progressive hypernatremia with Na 157 mmol/L; serum osmolality 367 mOsm/kg with inappropriately dilute urine. Differential diagnoses included central diabetes insipidus and osmotic diuresis, but preserved hemodynamics, normoglycemia, and normal calcium favored transient AVP-R due to tubular dysfunction and medullary washout. Desmopressin was withheld after physiologic correlation confirmed renal resistance. Gradual free-water replacement limited sodium correction to ≤ 12 mmol/L per 24 h. Sodium normalized, urine output stabilized and renal function recovered without dialysis or neurologic sequelae. Discussion This case illustrates a biphasic renal course—oliguric ATN followed by polyuric AVP-R—reflecting dynamic tubular recovery physiology. Regenerating epithelium expresses reduced aquaporin-2 channels, while medullary solute washout impairs urine concentration, producing transient vasopressin resistance. Clinically, AVP-R should be suspected in ICU patients who develop polyuria and hypernatremia during AKI recovery. Empiric desmopressin should be avoided until arginine vasopressin deficiency (AVP-D) is excluded, and sodium correction should not exceed 10-12 mmol/L/day. Conclusion Transient AVP-R is a reversible, under recognized cause of ICU-associated hypernatremia during ATN recovery. Early physiologic recognition, adherence to KDIGO electrolyte guidelines, and careful free-water replacement prevent neurologic injury and support full renal recovery. Recognizing transient AVP-R prevents unnecessary desmopressin use and osmotic demyelination, exemplifying the value of physiology-based management in critical care. This abstract is funded by: None