Abstract: FR-PO0884
Transient Postpartum Gestational Diabetes Insipidus Associated with Preeclampsia and Acute Transaminase Elevation
Session Information
- Fluid, Electrolyte, and Acid-Base Disorders: Case Reports - 1
October 23, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Fluid, Electrolytes, and Acid-Base Disorders
- 1102 Fluid, Electrolyte, and Acid-Base Disorders: Clinical
Authors
- Wang, Jiayan, University Hospitals Health System, Cleveland, Ohio, United States
- Garcia, Rafael, University Hospitals Health System, Cleveland, Ohio, United States
Introduction
Gestational diabetes insipidus (GDI) is a rare pregnancy-associated disorder caused by excess placental vasopressinase activity, resulting in accelerated degradation of vasopressin and development of hypotonic polyuria. Because vasopressinase is metabolized by the liver, hepatic dysfunction may impair its clearance and precipitate GDI. We report a case of transient postpartum GDI associated with preeclampsia and acute transaminitis.
Case Description
A 32-year-old woman presented 2 days after vaginal delivery at 36 weeks and 2 days gestation with dyspnea and bilateral lower extremity edema. She had no past medical history. Blood pressure was 165/88 mmHg. Examination demonstrated 2+ bilateral lower extremity edema. Initial laboratory studies showed sodium 142 mmol/L, potassium 2.7 mmol/L, ALT 88 U/L, AST 82 U/L. CT angiography showed cardiomegaly and pulmonary edema. She was diagnosed with postpartum preeclampsia with severe features and treated with intravenous magnesium sulfate and furosemide 20 mg. Her hospital course was complicated by two generalized tonic-clonic seizures consistent with eclampsia, which resolved with intravenous benzodiazepines. Liver enzymes peaked at ALT/AST 135/86 U/L. She subsequently developed marked hypotonic polyuria (osmolality 252 mOsm/kg) approaching 10 L/day. Severe hypokalemia persisted despite agressive potassium replacement and was attributed to renal potassium wasting from high distal tubular flow. Renin and aldosterone levels were suppressed. Given concern for gestational DI, intravenous desmopressin 0.52 mcg was administered, resulting in increased urine osmolality to 440 mOsm/kg and normalization of urine output. Hypokalemia resolved following correction of polyuria. Copeptin level obtained prior to desmopressin was normal at 12.2 pmol/L (reference ≤13.7). Sheehan syndrome was excluded by normal pituitary imaging and prolactin level. At 1-week follow-up, polyuria had resolved and electrolytes remained normal.
Discussion
This case highlights the diagnostic challenge of GDI in patients with postpartum polyuria, particularly after diuretic exposure. Hepatic dysfunction associated with preeclampsia may reduce vasopressinase clearance and exacerbate vasopressin deficiency. The rapid response to desmopressin supported GDI. Copeptin measurement may aid differentiation from nephrogenic DI, in which copeptin levels are generally elevated.