Abstract: TH-PO357
Plentiful Peeing in Pregnancy: Could It Be Potassium?
Session Information
- Sodium, Potassium, and Volume Disorders: Clinical
October 24, 2024 | Location: Exhibit Hall, 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
- Sundaram, Sruthi, Emory University School of Medicine, Atlanta, Georgia, United States
- Waheed, Sana, Emory University School of Medicine, Atlanta, Georgia, United States
Introduction
In pregnant patients with polyuria, it is important to consider diabetes insipidus (DI). To highlight this, we present a case of complete nephrogenic DI in pregnancy.
Case Description
A 15-year-old G1P0 female with gestational hypertension was admitted at 35 weeks of gestation with polyuria, polydipsia, and in preterm labor. She had persistent hypokalemia during pregnancy which was attributed to vomiting. Ongoing hypokalemia K < 3.0 meq/L and hypernatremia Na > 145 meq/L were noted. Urine output was 5-7 L per day. Plasma renin activity and aldosterone were normal. Urine osmolality was < 100 mosm/L and urine potassium was < 10 mEq/L. Desmopressin (DDAVP) test revealed complete arginine vasopressin-resistance (AVP-R) (Figure 1). Common causes were ruled out, and AVP-R was deemed most likely due to prolonged severe hypokalemia. The patient delivered a healthy preterm infant at 36 weeks, her vomiting resolved, and her serum potassium normalized with supplementation. However, her polyuria persisted, and a thiazide diuretic was initiated until it resolved.
Discussion
The original leading differential was gestational DI caused by placental production of vasopressinase and AVP breakdown; however, this would cause AVP-deficiency and is at odds with the result of the DDAVP test. Hypokalemia causes autophagic degradation of aquaporin-2 and decreased response to AVP causing AVP-R. Typically, the concentrating defect is mild, and symptomatic polydipsia and polyuria is rare. Our patient likely had severe degradation of aquaporin-2 caused by months of persistent hypokalemia resulting in complete AVP-R. Potassium supplementation was unsuccessful until after delivery due to intractable vomiting. Since there is data regarding safety of thiazides while breastfeeding, that was used to treat her persistent AVP-R postpartum. This case highlights the importance of considering nephrogenic DI in pregnant patients with polyuria and that the DDAVP test can be carried out safely. Fortunately, our patient only required treatment with a thiazide diuretic for 6 weeks postpartum, retained her ability to breastfeed her infant, and was able to be taken off treatment after resolution of AVP-R in a consistently normokalemic state.