Version May 2024
| Central DI in pregnancy | Nephrogenic DI in pregnancy | Transient DI of pregnancy | |
| Associations | Sheehan syndrome (postpartum hypopituitarism), surgical trauma, head trauma, pituitary adenoma, autoimmune or other infiltration, idiopathic, AVP gene mutation, Wolfram syndrome, anorexia nervosa, toxin (alcohol, snake venom) | AVPR2 and Aquaporin-2 gene mutations, lithium toxicity, medullary cystic kidney disease, polycystic kidney, hypokalemia, hypercalcemia, sickle cell disease or trait | May be associated with preeclampsia and/or liver abnormalities. Can result in postpartum DI due to placental abruption resulting in release of vasopressinase. |
| Vasopressin sensitivity: Pathophysiology | Sensitive: Decreased secretory reserve of ADH from pituitary; ADH levels may be further decreased by clearance by placental vasopressinase | Resistant: Renal resistance to ADH | Sensitive: Increased placental vasopressinase mediated clearance of ADH |
| Timing of presentation | May present in any trimester, may be recurrent | May present in any trimester, may be recurrent | Typically presents in the third trimester, though symptoms may be as early as fourth week of gestation; rarely occurs postpartum (placental abruption) |
| Diagnosis: Response to DDAVP administration | Urine osmolality normalized | No change to urine osmolality | Urine osmolality normalized |
| Diagnosis: Plasma ADH level | Low to absent | Normal to high | Low to absent |
| Management | Responds to DDAVP | May be resistant to both ADH and DDAVP; consider hydrochlorothiazide or amiloride | Responds to DDAVP, resistant to ADH |
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