Case Presentation:

A 15–year–old primigravida with no prenatal care at 32 weeks of gestation presented with preterm contractions, abdominal pain, elevated BP and headache. An elevated sodium of 153 mEq/L was initially believed to be the result of dehydration. After IV hydration with normal saline serum sodium continued to rise and was 160 mEq/L in 24 hours. Hospitalist was now consulted. Due to the elevated BP pregnancy induced hypertension(PIH)was suspected and standard PIH labs were ordered which were negative. Work up for DI was initiated at this point. Baseline serum sodium was 160 mEq/L, serum osmolality was 326 mOsm/kg, urine sodium was 27 mEq/L and urine osmolality was 84 mOsm/kg prior to a DDAVP(Desmopressin) challenge. Evaluation for central vs nephrogenic DI was performed with DDAVP 2 mcg intramuscularly(IM). A serum sodium of 150 mEq/L and urine osmolality of 180 mOsm/kg was seen 2 hours later. Since the urine osmolality had more than doubled a central DI was suspected. MRI of the brain did not show any pituitary mass. Serum anti–diuretic hormone(ADH) was below detectable levels. DDAVP was held but despite the patient taking in 3 l of oral free water in 24 hours her serum sodium and osmolality returned to abnormally high values and her urine sodium and osmolality returned to abnormally low levels. She was diagnosed with Gestational–associated diabetes insipidus(GDI)secondary to increased vasopressinase activity. DDAVP was restarted and her serum and urine sodium and osmolality normalized further supporting our diagnosis. Discussion: DI is characterized by polydipsia, polyuria and hypotonic urine. Central DI is due to defective synthesis or release of arginine–vasopressin (AVP) or ADH from the hypothalamo–pituitary axis. Nephrogenic DI is due to renal insensitivity to AVP. GDI is seen in the third trimester affecting between two and six cases per 100,000 pregnancies. Normally sodium decreases by 5 meq/L early in pregnancy due to a lower threshold for ADH release, increased thirst, and volume dilution effects. This is caused by the increase in human chorionic gonadotropin. In normal pregnancy the enzyme vasopressinase released from the placenta maintains fluid balance by increasing ADH clearance. Elevated levels of vasopressinase cause the degradation of ADH leading to GDI.

Conclusions:

GDI presents in different ways and is difficult to diagnose based on symptoms alone. Routine screening is unnecessary and not cost effective but it should be considered as a diagnosis when more common causes for hypernatremia have been ruled out. The treatment of choice is DDAVP IM injection.

Figure 1GDI – Serum Sodium.

Figure 2GDI – Urine Osmolality.