Gestational Diabetes Insipidus (GDI) is a rare complication in pregnancy. It is a transient process secondary to vasopressinase production and release from placental trophoblasts. This may result in decreased circulating arginine vasopressin despite appropriately increased endogenous production from the posterior pituitary gland.
A 31-year-old woman, G4P2, presented at 33 weeks gestation with a five-day history of polydipsia and polyuria. She has a past medical history of migraines; she was taking was pregnancy multivitamins only. Initial evaluation demonstrated a serum sodium 139 mmol/L (135-145), serum osmolality 280 mOsmol/kg (275-295), and urine osmolality 239 mOsmol/kg (300-900). She was normotensive 120/77mmHg, had normal liver transaminases and anterior pituitary hormone levels. Her 24hr urine output was 4.1. Foetal assessment was normal including ultrasonography. A water deprivation test was undertaken with strict safety endpoints. She had near-normal capacity to concentrate urine (endpoint urine osmolality 648 mOsmol/kg, serum sodium 139 mmol/L and serum osmolality 279 mOsmol/kg). She had an excellent clinical response to desmopressin 100mg orally.
Despite inconsistent biochemical markers, her clinical presentation was strongly suggestive of GDI. She discharged home on desmopressin and remained well until 38 weeks plus 2 days of gestation. She represented with worsening polyuria despite desmopressin. Unfortunately, her desmopressin was not titrated due to persistently normal serum sodium levels. She became mildly hypertensive, 132/87mmHg, and had mildly elevated alkaline phosphatase of 134 U/L (30-110). Foetal ultrasonography demonstrated oligohydramnios. She underwent induction of labour (IOL) for reduced foetal movement. Her desmopressin was ceased day of delivery, however, she was re-admitted 48 hours post discharge with ongoing polyuria and clinical dehydration. Recommencement of desmopressin resolved all symptoms. It was ceased eight weeks postpartum and she remains well.
This case report highlights the importance of diagnosing and treating patients with clinical symptoms of GDI despite inconsistent baseline biochemistry to minimise maternal and foetal complications.