Abstract
Background: Gestational diabetes insipidus (GDI) is a rare but recognized complication of pregnancy. We are reporting the case of a 33-year-old patient who presented in her 3rd trimester with GDI, severe asymptomatic hypokalemia & hypomagnesemia. This presentation of GDI has not been reported yet to our knowledge.
Clinical Case: A 33-year-old G2P1 patient who presented to the hospital due to the discovery of new onset severe asymptomatic hypokalemia on routine labs. Further evaluation revealed K of 2.8 mEq/L, Mg of 1.4 mg/dL & Na of 142mEq/L. She endorsed polyuria & polydipsia and a 24-hour urine collection of 9.35L confirmed diabetes insipidus. Labs also revealed a serum osmolality of 286mOsm/kg & urine K of 15mEq/L. Her urine osmolality was inappropriately low at 138mOsm/kg. She received K & Mg supplementation. In pregnant patients suspected of having GDI who have normal serum Na, water restriction test can be done for further evaluation. It must performed with close monitoring because dehydration can lead to uteroplacental insufficiency. Given her history of previous fetal demise & report of headaches with attempts of water restriction, we opted not to do the test. She was given subcutaneous 1 mcg of desmopressin overnight with her thirst & polyuria improving only briefly. Due to her suboptimal response, we began her on 10 mcg of intranasal spray of desmopressin once in the evening. Her symptoms resolved on this regimen after a few days of observation. Her Mg & eventually K levels reached and remained at normal levels after repletion. The rest of her pregnancy went on without complications and she delivered a healthy male infant via scheduled cesarean section at 36 weeks gestation. She discontinued intranasal desmopressin after 2 weeks and has remained asymptomatic. Labs at follow up 4 weeks later remained normal. It is known that vasopressinase which is made by placental trophoblasts during pregnancy degrade endogenous ADH1. We are hypothesizing that since ADH has been shown to be effective in conserving magnesium in rats by stimulating its uptake in the distal convoluted tubule cells2, a similar mechanism could be present in humans. We believe that the loss of endogenous ADH, leads to the depletion of Mg and consequently hypokalemia in susceptible patients.
Conclusion: To our knowledge this is the first case presenting the possible role of vasopressinase in the development of hypomagnesemia & hypokalemia in a patient with GDI.
Reference: 1. Gordge MP, Williams DJ, Huggett NJ, Payne NN, and Neild GH. Loss of biological activity of arginine vasopressin during its degradation by vasopressinase from pregnancy serum. Clinical Endocrinology, vol. 42, no. 1, pp. 51- 58, 1995. 2. Dai LJ, Bapty B, Ritchie G, Quamme GA. Glucagon and arginine vasopressin stimulate Mg2+ uptake in mouse distal convoluted tubule cells. Am J Physiol. 1998 Feb;274(2):F328-35. doi: 10.1152/ajprenal.1998.274.2.F328. PMID: 9486227.
The clinical course and pathophysiological investigation of adolescent gestational diabetes insipidus: a case report