SAT-140 Case Report: Gestational Diabetes Insipidus Caused by Cholestasis of Pregnancy

Abstract Disclosure: S.D. Mohan: None. Introduction:This is a unique case of diabetes insipidus (DI) presenting as a complication of cholestasis of pregnancy. We will review the pathophysiology and treatment of gestational DI. Clinical case:A 37-year-old Caucasian female G2P1 with Dichorionic Diamniotic (DCDA) twins presented to hospital at 33 weeks’ gestation with premature uterine contractions. She complained of sudden onset of increased thirst and urine output over the preceding 24 hours, drinking 5.5 litres. Her past history was significant for diet controlled gestational diabetes, iron deficiency and an uneventful first pregnancy. She was clinically hypovolemic with reduced skin turgor and hypotension. A serum sodium was 139 (135-145) mmol/L, serum osmolality 292 (275-295) mmol/Kg, urine sodium 66 (40-220) mmol/L and urine osmolality 235 (350-1000) mmol/Kg . Her glucose levels were well controlled. Her liver function panel was consistent with cholestasis of pregnancy with elevated bile acids 68umol/L (0-6) and no anatomical obstruction on liver ultrasound. She was commenced on ursofalk 500mg three times daily. A comprehensive assessment of the pituitary axis and Magnetic resonance imaging (MRI) of the pituitary gland was unremarkable. A single dose of oral desmopressin (DDAVP) 200mcg was given with rapid improvement in urine output within 1 hour, reducing from 300ml/hr to 75ml/hr. Urine output improved to 1.1L over 24hours. A repeat serum sodium 24hrs after DDAVP was 136mmol/L and serum osmolality 284mmol/kg. Due to worsening liver function, she underwent an emergency caesarean section. The patient and both neonates made a full recovery post-partum. Discussion: Gestational DI or transient DI in pregnancy is rare, occurring in 2-4/100 000 pregnancies. It occurs due to increased placental syncytiotrophoblast production of vasopressinase which rapidly breaks down vasopressin. This is different from central DI and nephrogenic DI; although these conditions can also be exacerbated in pregnancy. Production of vassopressinase increases through pregnancy up to 1000-fold in the 3rd trimester, with greater production in patients with larger placental volume and reduced clearance in patients with liver dysfunction. Gestational DI may be missed as polyuria is often dismissed as a normal part of pregnancy but if untreated can cause severe dehydration and uteroplacental deficiency adversely affecting both mother and baby. Confirming the diagnosis requires monitoring of fluid input and output and paired serum and urine sodium and osmolality. It is best to avoid water deprivation testing due to the risks of dehydration in pregnancy. An MRI pituitary will help to confirm the presence of the posterior pituitary bright spot and similarly a copeptin level can help distinguish gestational DI from cranial DI. DI may be managed safely in pregnancy with use of vasopressin analogues such as DDAVP and will resolve after delivery. Presentation: Saturday, July 12, 2025