Poster Presentation The Joint Annual Scientific Meetings of the Endocrine Society of Australia and the Society for Reproductive Biology 2017

Transient diabetes insipidus in a postpartum woman with preeclampsia associated with residual placental vasopressinase activity (#280)

Natassia Rodrigo 1 , Samantha Hocking 1
  1. Endocrinology, Royal North Shore Hospital, St Leonards, NSW, Australia

A 48-year-old lady presented with a 3 day history of worsening, global headache, associated with bilateral leg swelling, polydipsia, polyuria and nocturia. Of note, she was 8 days post-partum, having delivered by elective lower segment caesarean section (LSCS). This last pregnancy was achieved through IVF. She had no other significant past medical or family history of disease and was not on any regular medications. On examination, she was hypertensive to 183/87mmHg, with brisk reflexes. Cranial nerve examination was normal. Cardiovascular examination noted bilateral pitting oedema and dry mucous membranes. Investigations revealed an enlarged pituitary on CT, proteinuria with protein: creatinine ratio 110 mg/mmol, sodium of 146mmol/L, creatinine 150umol/L, eGFR 35, urate 0.58mmol/L (0.15-0.40) and mildly deranged liver function tests. Her urine osmolality was 175mmol/Kg with a serum osmolality of 308mmol/Kg. She underwent a water deprivation test, which terminated after 4 hours, with sodium rising to 146mmol/L with a serum osmolality of 302mmol/Kg and urine 175mmol/Kg. Her Anti-diuretic hormone (ADH) level was <0.8ng/L. Her anterior pituitary hormone profile was normal. She was diagnosed with post-partum pre-eclampsia and diabetes insipidus secondary to residual placental vasopressinase. By one month post discharge her symptoms had resolved with resolution of both her pre-eclampsia and diabetes insipidus, such that she no longer required any medications.

Transient Diabetes insipidus (DI) is rare complication of pregnancy, secondary to increased placental vasopressinase activity[1]. Post-partum presentations are exceedingly unusual[1]. Post-partum DI has previously been described in relation to placental abruption, due to large volume release of placental vasopressinase into the blood stream[2]. It can be hypothesised that placental manipulation, through LSCS, can lead to similar release of vasopressinase, precipitating DI. Vasopressinase concentrations are commensurate with placental mass. IVF pregnancies are associated with larger placental weights, and thus increased risk of transient DI [3].

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