Pregnancy is associated with a lowering of the osmostat, the setpoint for plasma osmolality at which arginine vasopressin (AVP) is secreted, by ˜10 mOsm/kg. Thus, pregnant women experience thirst and release AVP at lower levels of plasma osmolality than do nonpregnant women.1 The physiologic basis for this reset osmostat is not clear, but some studies suggest that it is related to high levels of human chorionic gonadotropin (hCG).1 In a patient with polyuria and polydipsia, therefore, the finding of lower than expected serum sodium levels should not exclude the diagnosis of diabetes insipidus (DI).2 Testing of urinary concentrating ability (see Chap. 25 and Chap. 26) in a pregnant woman should be performed with the patient in the sitting position, because the lateral recumbent position results in an inhibition of maximal urinary concentrating ability.1,2

The placenta produces vasopressinase, an enzyme that inactivates AVP rapidly. Vasopressinase levels increase 1000-fold between the 4th and 38th weeks of gestation.3 This increased metabolic clearance of AVP interferes with the determination of plasma AVP levels during pregnancy and may explain the blunted rise in these levels seen during hypertonic saline infusion in the last trimester.1 Therefore, nomograms that indicate “normal” relationships between plasma osmolality and AVP for nonpregnant patients cannot be used for pregnant patients.