Abstract: FR-PO0997
Transient Vasopressinase-Mediated Postpartum Diabetes Insipidus Responsive to Desmopressin Acetate (DDAVP)
Session Information
- Women's Health and Kidney Diseases
October 23, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Women's Health and Kidney Diseases
- 2100 Women's Health and Kidney Diseases
Authors
- Shah, Shreya M., University of Maryland Baltimore School of Medicine, Baltimore, Maryland, United States
- Regenold, David Klaus, University of Maryland Baltimore School of Medicine, Baltimore, Maryland, United States
- Ijaz, Nadia, University of Maryland Medical System, Baltimore, Maryland, United States
- Phan, Tramanh, University of Maryland Medical System, Baltimore, Maryland, United States
- Khan, Sarah Hussain, University of Maryland Medical System, Baltimore, Maryland, United States
Introduction
Transient postpartum diabetes insipidus (DI) is a rare complication of hypertensive disorders of pregnancy, especially with placental abruption and hepatic dysfunction. Diagnosis is challenging when polyuria overlaps with AKI and physiologic postpartum diuresis.
Case Description
A 28-year-old G3P1111 with chronic hypertension developed superimposed preeclampsia with severe features complicated by placental abruption, intrauterine fetal demise at 32 weeks, and DIC requiring emergent cesarean delivery. Her postpartum course was complicated by severe oliguric AKI and hyperkalemia following hemorrhage and hypoperfusion. As renal function improved, she developed marked polyuria with low urine osmolality and impaired urine concentration despite free water losses (Figure 1). DDAVP reduced urine output and improved symptoms. With supportive care and fluid/electrolyte management, her kidney function improved and urine output stabilized.
Discussion
Transient postpartum DI results from excess placental vasopressinase, which may persist after delivery in preeclampsia due to impaired hepatic clearance, causing vasopressin degradation, polyuria, impaired urinary concentration, and dilute urine responsive to desmopressin. Although concurrent AKI was present in our patient, post-ATN diuresis typically has an osmotic solute component, whereas DI causes free water diuresis. Significant oral water intake and continuous IV fluids can mask overt hypernatremia despite ongoing renal free water losses. Delayed recognition may worsen volume depletion and electrolyte abnormalities. Early urine osmolality assessment and a desmopressin trial are critical for diagnosis and management. This case highlights the importance of recognizing postpartum DI in patients with disproportionate polyuria after hypertensive disorders of pregnancy.
Acknowledgment
We thank the clinical teams involved in the patient’s care for their support in this case report.
Figure 1. Temporal Trends in Urine Output, Osmolality, and Renal Function During Postpartum AKI and Transient DI Recovery.