Version July 2025
| AVP deficiency | AVP resistance | Transient AVP deficiency of pregnancy | |
| Associations | Sheehan syndrome (postpartum hypopituitarism), surgical trauma, head trauma, pituitary adenoma, autoimmune or other infiltration, idiopathic, AVP gene mutation, Wolfram syndrome | AVPR2 and Aquaporin-2 gene mutations, lithium toxicity, chronic kidney disease, hypokalemia, hypercalcemia, sickle cell disease or trait | Associated with preeclampsia and liver disease. Placental abruption can lead to postpartum AVP-D due to release of vasopressinase. |
| Pathophysiology | Decreased secretion of AVP from pituitary; AVP levels may be further decreased by placental vasopressinase | Renal resistance to AVP | Placental vasopressinase increases breakdown of AVP |
| 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) |
| Response to DDAVP administration | Urine osmolality increases | No or a modest change in urine osmolality | Urine osmolality increases |
| Plasma AVP level | Low to absent | Normal to high | Low to absent |
| Management | Responds to desmopressin | Resistant to desmopressin. A low-protein, low-sodium diet may help polyuria. Other treatments for nonpregnant patients (eg, thiazide diuretics, nonsteroidal anti-inflammatory agents) are typically avoided in pregnancy. | Responds to desmopressin (not metabolized by vasopressinase) |
