A 41-year-old pregnant woman with a known history of human immunodeficiency virus (HIV) infection and chronic hepatitis B virus (HBV) infection presented for routine follow-up in January 2020. Her past HIV history was notable for poor adherence to antiretroviral therapy (ART), a diagnosis of acquired immunodeficiency syndrome in 2009, and prior hospitalizations for presumed cytomegalovirus (CMV) encephalitis and Kaposi sarcoma. She reported no history of alcohol consumption, tobacco use, or illicit drug intake. Her obstetric history included one previous uncomplicated pregnancy.

Six months prior to presentation, she had restarted ART consisting of tenofovir 245 mg/day, emtricitabine 200 mg/day, and dolutegravir 50 mg/day, which initially resulted in satisfactory virological control and no laboratory abnormalities. However, she subsequently missed scheduled follow-up appointments and had discontinued her medications approximately one month prior to this visit. At the time of presentation, she was 22 weeks pregnant and reported persistent malaise for three weeks.

On physical examination, the patient was hypotensive (BP: 87/61 mmHg) and bradycardic (heart rate 61 beats/min), with an oxygen saturation of 96% on room air. Clinical assessment revealed reduced skin turgor, disorganized speech, and cerebellar signs, including ataxia and dysmetria on finger-to-nose testing. Given these findings, she was transferred to the emergency department for further evaluation.
Laboratory investigations demonstrated mild anemia (hemoglobin 101 g/L), new-onset renal impairment (serum creatinine 118 µmol/L; blood urea nitrogen 19 mmol/L), and hyperosmolar hypernatremia (serum sodium 161 mmol/L; plasma osmolality 322 mOsmol/kg). Serum glucose, potassium, and calcium levels were within normal limits. Urinalysis showed a urine specific gravity of 1.013, and 24-hour urinary studies revealed low urine osmolality (216 mOsmol/kg). Plasma copeptin levels were elevated (22.68 pmol/L). Endocrine evaluation demonstrated normal thyroid function, cortisol, and adrenocorticotropic hormone (ACTH) levels. Brain MRI revealed white matter hyperintensities without evidence of pituitary abnormalities. Renal ultrasonography demonstrated globose kidneys. Virological assessment showed an HIV viral load of 2,300,000 copies/mL with a CD4+ T-cell count of 426 cells/µL. Obstetric ultrasonography identified oligohydramnios and a fetus with pulmonary hypoplasia measuring at the 9th percentile for gestational age. Based on the clinical and laboratory findings, a diagnosis of gestational diabetes insipidus was made, likely representing unmasking of underlying subclinical nephrogenic DI, potentially related to HIV-associated nephropathy or prior tenofovir exposure. Treatment with desmopressin was initiated at 0.06 mg/day, later increased to twice daily dosing. Following therapy, serum sodium and plasma osmolality normalized, accompanied by improvement in neurocognitive symptoms. Due to progressive fetal deterioration, the pregnancy was terminated at 24 weeks of gestation. Desmopressin therapy was discontinued after delivery. At 5-month follow-up, copeptin levels remained elevated; however, there was no recurrence of diabetes insipidus symptoms.