Arginine Vasopressin Deficiency Concealed by Progressive Kidney Injury

Background Arginine vasopressin deficiency (AVPD), formerly central diabetes insipidus, is characterized by polyuria and hypernatremia due to inadequate vasopressin production. Most cases are acquired—commonly after pituitary surgery or hypothalamic injury—and require lifelong desmopressin therapy. We report a case of long-standing AVPD in which progression to severe kidney failure and dialysis masked classical manifestations, creating the appearance of disease resolution. Case Presentation A 67-year-old woman with AVPD secondary to olfactory groove meningioma resection had required high-dose desmopressin for over 20 years, with prior hospitalizations for hypernatremia during missed doses. She also had chronic kidney disease (CKD) stage 3b. She presented with progressive confusion and was found to have severe acute kidney injury (creatinine 11 mg/dL), metabolic acidosis, hyperkalemia, and sepsis, ultimately requiring hemodialysis for uremic encephalopathy. Desmopressin was withheld on admission due to normal serum sodium; however, she remained oliguric (150–400 mL/day), and serum sodium and osmolality stayed within normal limits throughout hospitalization, with no biochemical or clinical evidence of AVPD. Discussion This case highlights that advanced kidney failure can mask AVPD. Impaired free water excretion and altered sodium handling in severe renal dysfunction may prevent hypernatremia, obscuring classical AVPD signs. Conclusion / Learning Point AVPD may become clinically silent in advanced kidney disease. Desmopressin therapy should not be considered dogmatic in this setting and may require careful reassessment.