SAT-002 - Unmasking Chronic Arginine Vasopressin Deficiency in the Setting of Intestinal Neobladder: A Case Report

Background: Arginine vasopressin, secreted by the posterior pituitary, regulates renal water reabsorption. Arginine vasopressin deficiency (AVP-D) typically causes hypernatremia, polyuria (> 3 L/day), polydipsia, and low urine osmolality ( < 200-300 mOsm/kg).

Case Presentation: A 53 year-old man with metastatic urothelial carcinoma, status-post radical cystoprostatectomy with ileal neobladder (3 years prior) and a recently diagnosed sellar mass causing panhypopituitarism presented with 3 weeks of progressive encephalopathy. Vitals were normal. Laboratory evaluation revealed chronic hyponatremia (130-134 mmol/L for 3 years). Infectious workup was unrevealing. Imaging revealed interval growth of sellar mass (3.1cm vs. 2cm), new supraclavicular lymphadenopathy, thoracic/abdominal nodal growth, and multiple new intrathecal lumbar masses consistent with metastatic progression. Biopsy confirmed metastatic high-grade urothelial carcinoma. Palliative radiation was initiated.

During his hospitalization, he was frequently NPO for anesthesia. Three weeks into admission, serum sodium rose to 155 mmol/L. Urine osmolality was inappropriately low at 333 mOsm/kg. These findings suggested AVP-D, however polyuria was absent (urine output was only 1-1.5L/day). We hypothesized that water reabsorption from the ileal neobladder tempered polyuria and stabilized urine osmolality. Desmopressin (DDAVP) was started; the initial dose showed no effect, but subsequent doses normalized sodium. Redosing was guided by serum sodium >145 or urine output >1L/day. He was weaned off high-dose 5% dextrose infusion and maintained normonatremia.

Discussion: Standard AVP-D criteria of polyuria and dilute urine were unreliable due to the neobladder-mediated water absorption and altered solute composition. Initial DDAVP non-response likely reflected chronic AVP-D with renal medullary concentration gradient washout and aquaporin downregulation. Based on published data, the 50 cm ileal segment used for neobladder construction may provide ~2L absorptive capacity; thus, we used >1L urine/day as polyuria in his case. The patient likely maintained water balance despite AVP-D until NPO status restricted water intake, limiting neobladder-absorption associated compensation. This compensatory mechanism highlights an underrecognized physiologic adaptation and opens exciting avenues for research in patients with adipsic AVP-D.

Conclusion: Conventional AVP-D evaluation using urine output and osmolality is unreliable in patients with intestinal neobladders.

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