FRI352 Diabetes Insipidus With Hypokalemia In A 30 Week Pregnant Female

Abstract

Abstract Disclosure: C.B. Stanfield: None. In this case, we will discuss a 29 year old G4P0121 African American female at 30 weeks gestation presented to women’s urgent care for nausea, vomiting and diarrhea after starting magnesium supplementation for incidentally diagnosed hypokalemia around 4 weeks prior. Vitals were significant for a BP of 133/60 and HR 110. Laboratory studies were significant for potassium of 3 mmol/L, sodium 155 mmol/L, magnesium 2.2mmol/L, AST 104, ALT 62 and UA with 2+ proteinuria. Patient admitted to the OBGYN service for preeclampsia with severe features. Patient was noted to have over 16L UOP over the first 24 hours of admission; 4.5L intake. Further labs obtained showed hemoglobin A1C of 4.9, serum osmolality of 308 mOsm/kg, urine osmolality 77 mOsm/kg and urine specific gravity 1.002. DDAVP was given with urine osmolality increasing from 77 to 137 mmol/L. Working differential diagnoses included gestational diabetes insipidus (DI), central DI or nephrogenic DI due to hypokalemia. Co-peptin assay was drawn; is a send out at our institution. Of note, the patient had no known history of brain injury, surgery, radiation or Sheehan Syndrome. However her previous pregnancies had been complicated by hypokalemia, hypertension and pre-eclampsia with emergent cesarean-section. She subsequently underwent emergency cesarean-section on hospital day 2 for non-reassuring fetal activity with delivery of viable 1230g male. After delivery, the patients hypokalemia resolved. Post-op, DDAVP for 3 days was continued per hospital DI protocol with appropriate response. Co-peptin resulted at 22.3, excluding central DI as a diagnosis. On time of discharge, patient had gone without DDAVP for >48 hours with intact thirst mechanism. Given improvement/resolution of DI and persistently low urine osmolality even after DDAVP administration prior to delivery, the DI was believed to be gestational with a component of nephrogenic DI as well due to hypokalemia. Gestational DI occurs due to increased placental vasopressinase which degrades the antidiuretic hormone (ADH). It is associated with pre-eclampsia, acute fatty liver of pregnancy and HELLP syndrome. DDAVP is a modified synthetic analog of endogenous ADH and is resistant to breakdown by placental vasopressinase and can be used to treat gestational DI. Definitive management is achieved with delivery of the fetus and can last up to six weeks after delivery. Presentation: Friday, June 16, 2023