Gestational diabetes insipidus is a rare, temporary pregnancy complication. It leads to increased urine output and more frequent urination due to the breakdown of a hormone called vasopressin.

Diabetes insipidus, also known as arginine vasopressin disorder (AVD), develops when the body becomes less able to respond to vasopressin or does not make enough of it. Vasopressin is a hormone that helps the body hold onto fluids. AVD means a person passes more urine, and their urine is paler and weaker than those without AVD.

Several types of AVD can develop depending on the underlying cause and how the body produces or interacts with vasopressin. Damage to the parts of the brain responsible for vasopressin, such as the pituitary gland, is often responsible. However, it can also occur during pregnancy, which is known as the gestational form of arginine vasopressin disorder (gAVP-D).

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The gestational form of arginine vasopressin disorder (gAVP-D) is a condition that leads to the destruction of vasopressin during pregnancy. In about 1 in every 30,000 pregnancies, gAVP-D occurs, meaning it is rare.

The condition develops when a person’s placenta cells, called trophoblasts, create an enzyme called vasopressinase. This enzyme breaks down vasopressin. As the pregnancy progresses, the number of trophoblasts increases by around 1,000 times, which can speed up vasopressin breakdown. This reduces how much water the individual reabsorbs.

Typically, gAVP-D tends to develop towards the end of the second trimester or during the third trimester.

However, according to a 2021 study, those who already had asymptomatic AVD before becoming pregnant may find their symptoms develop earlier in the pregnancy. They cannot replenish their vasopressin levels quickly enough to replace that which the trophoblasts break down.

The condition often resolves without active treatment around 4 to 6 weeks after delivery.

Although they both develop due to pregnancy, gestational diabetes mellitus (DM) and gAVP-D are different conditions. AVD interferes with fluid balance, whereas DM causes raised levels of a person’s blood sugar, or glucose.

Gestational DM leads to a buildup of glucose in the blood after the pregnant person’s cells become less responsive to the hormone, insulin. This hormone moves glucose from the blood to cells that need it. The causes of gestational DM are less clear than those of gAVP-D, although placental hormones might also play a role.

It is also far more common than gAVP-D, occurring in around 1 in 10 pregnancies in the United States.

Pregnancy is the main cause of gAVP-D. However, pregnancies with multiple fetuses, such as twins or triplets, increase the risk of gAVP-D, as more placental tissue develops.

The condition also has a link to pregnancy-related conditions that affect the liver, as the liver helps block vasopressinase. Examples include preeclampsia — pregnancy-linked high blood pressure — and hemolysis, elevated liver enzymes, and low platelets (HELLP) syndrome.

Symptoms of gAVP-D resemble those of other types of AVD. These include:

  • feeling extremely thirsty and needing to regularly drink fluids
  • peeing often, even during the night
  • passing a high volume of light-colored urine

One gAVP-D complication is dehydration. According to a 2023 study, dehydration may have links to adverse pregnancy outcomes, including adverse effects on the infant’s birth weight, birth length, and head and chest circumference. Managing gAVP-D may reduce the risk of dehydration.

A 2020 review also suggests high blood sodium, resulting from gAVP-D, can reduce how effective anesthetic medications are during the delivery of an infant.

Doctors often underdiagnose gAVP-D, as pregnancy generally causes more frequent urination without leading to complications.

Water deprivation tests, which involve withholding water for several hours and measuring urine output, are usually the gold standard for diagnosing AVD. However, according to a 2018 case study, water deprivation may potentially harm the growing fetus.

A 2021 study suggests doctors do not routinely use the water deprivation test during pregnancy anymore due to its limited accuracy but recommends close monitoring when doctors do administer the test.

Several other methods can help a doctor rule out other causes of excessive urination during pregnancy:

  • urine tests to measure how diluted the urine is
  • blood tests to assess sodium levels
  • MRI scans to check for physical damage to the hypothalamus or pituitary gland

Desmopressin is often the most suitable treatment for gAVP-D. It is a synthetic version of vasopressin.

Desmopressin replaces vasopressin, which helps increase water retention. However, the placental cells do not break down desmopressin as they do vasopressin. Importantly, desmopressin is also safe for both the pregnant person and the fetus.

By controlling symptoms, a person with gAVP-D can prevent complications. This type of AVD often resolves 4 to 6 weeks after delivery but may return during future pregnancies.

The gestational form of arginine vasopressin disorder (gAVP-D) is a rare pregnancy complication. It occurs when cells in the placenta break down vasopressin, increasing the frequency of urination and the volume of urine. It usually develops from the end of the second trimester onward. Pregnancy-related liver problems and having multiple fetuses can increase the risk of gAVP-D.

Testing for gAVP-D may not always include a water deprivation test, which is the standard test for diagnosing types of arginine vasopressin disorder (AVD). Instead, blood and urine testing can help identify sodium levels and urine concentration. Individuals can take desmopressin, a lab-made vasopressin substitute, to treat gAVP-D. The condition often resolves shortly after pregnancy but might recur during future pregnancies.