Metabolic Management
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June 28, 2024

What is Diabetes Insipidus?

Medically Reviewed by
Updated On
September 17, 2024

Diabetes insipidus (DI) is caused by a deficiency of antidiuretic hormone (ADH) or an insensitivity to its effects. This leads to an inability to conserve water, which results in excessive thirst (polydipsia) and the excretion of large volumes of dilute urine (polyuria).Β 

Timely diagnosis and effective management of DI are essential to prevent complications such as dehydration and electrolyte imbalances. This article aims to provide a comprehensive overview of DI, its symptoms, diagnosis, and treatment options to enhance awareness and improve patient outcomes.

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What is Diabetes Insipidus?

When there is a deficiency in ADH or a reduced kidney response to ADH, the body suffers an imbalance in fluid regulation due to an inability to retain water effectively. This results in excessive thirst (polydipsia) and the production of large volumes of dilute urine (polyuria) that characterizes diabetes insipidus. In DI, urine output is typically excessive, often exceeding 3 liters in 24 hours, with a very dilute concentration of osmolality less than 300 mOsm/kg.

Milestones in Understanding Diabetes Insipidus

The scientific understanding of DI has evolved significantly over several centuries since its first clinical description in the 18th century when patients were observed to have excessive thirst and urination without elevated blood glucose levels. In the early 20th century, researchers identified the hormone vasopressin (also known as ADH) and began to understand its important role in regulating water balance, bringing to light the intricacies of water balance in the body.Β 

Differentiation from Diabetes Mellitus

While the names sound similar, diabetes insipidus and diabetes mellitus involve different hormonal imbalances and causes. Diabetes derives from the Greek word siphon, referring to urine, or the fluid filtered out by the kidneys. While both conditions cause frequent urination and excessive thirst, these symptoms are caused by distinct underlying mechanisms.

Excessive dilute urine occurs in DI due to ADH insufficiency or resistance that causes impaired water retention. On the other hand, in diabetes mellitus, impaired insulin production results in impaired glucose metabolism and high blood sugar levels that contribute to excessive thirst and urination.Β 

Epidemiology of Diabetes Insipidus

DI is relatively rare, with an estimated prevalence of about 1 in 25,000 individuals. This condition occurs worldwide, with no specific geographic or ethnic predilection. There is no significant gender difference in the prevalence of DI, although some forms may show slight variations based on genetic factors.

DI can affect individuals of any age, but certain forms may have specific demographic patterns. DI arising from an issue with pituitary production of ADH (central DI) often arises in childhood or young adulthood, while DI occurring due to reduced kidney response to ADH (nephrogenic DI) can be congenital or acquired later in life.Β 

Causes of Diabetes Insipidus

DI results from either a deficiency in ADH production (central DI) or a reduced kidney response to ADH (nephrogenic DI). ​​

Central Diabetes Insipidus

Central DI, also referred to as arginine vasopressin (AVP)-deficiency, is the most common form of DI resulting from deficiency of the hormone AVP being released from the pituitary gland.Β 

Idiopathic Central DI

Idiopathic central diabetes insipidus occurs when the deficiency in ADH production occurs with no identifiable underlying condition or obvious damage to the hypothalamus or pituitary gland.

Secondary Central DI

When identifiable damage to the hypothalamus or pituitary gland, such as from pituitary tumors, head trauma, autoimmune attack, infections, or surgeries, results in DI this is classified as secondary central diabetes insipidus. This damage to the posterior pituitary gland impairs ADH production, leading to symptoms of DI.

Nephrogenic Diabetes Insipidus

The less common nephrogenic DI occurs when resistance develops in the kidneys, causing them not to respond sufficiently when stimulated with ADH.

Inherited Nephrogenic DI

Inherited or hereditary nephrogenic DI is a genetic disorder where the kidneys are unable to respond to ADH. Normally, ADH binds to its type-2 receptor (AVPR2 )in the kidneys' collecting duct, causing the exocytosis of the water channel aquaporin 2 (AQP2) at the apical membrane, allowing water to be reabsorbed. Inherited nephrogenic DI results due to mutations in the AVPR2 gene or AQP2 gene, affecting the receptors or channels necessary for water reabsorption.

Acquired Nephrogenic DI

Acquired nephrogenic DI occurs when external factors such as certain medications (e.g., lithium), chronic kidney disease, or electrolyte imbalances (e.g., hypercalcemia, hypokalemia) impair the kidneys' response to ADH.

Dipsogenic Diabetes Insipidus

Primary Dipsogenic DI

Primary dipsogenic DI is a type of primary polydipsia involving an abnormal increase in thirst and fluid intake. This condition is due to a malfunction in the thirst mechanism in the hypothalamus, leading to excessive drinking and subsequent dilution of urine.

Secondary Dipsogenic DI

Secondary dipsogenic DI occurs due to brain injuries, surgeries, or diseases affecting the hypothalamus or other areas that regulate thirst. These injuries cause abnormal stimulation of thirst, leading to excessive fluid intake and diluted urine.

Gestational Diabetes Insipidus

Gestational DI occurs during pregnancy, often in the third trimester, due to increased metabolism of ADH by placental enzymes (vasopressinase) and sometimes due to increased ADH clearance. It is usually transient during pregnancy.

Symptoms of Diabetes Insipidus

Due to the inability of the kidneys to concentrate urine adequately, common symptoms of DI include:

In infants and children, symptoms of DI may manifest as irritability, poor feeding, failure to thrive, dehydration, dry skin, sunken fontanelles (soft spots on the head), lethargy, and delayed growth.Β 

Pathophysiology

ADH, also known as vasopressin, is a hormone released from the posterior pituitary gland that normally helps the kidneys retain water by concentrating urine.Β 

Dysfunction in the neurohypophyseal pathway involves impaired synthesis, release, or action of ADH in the hypothalamus or posterior pituitary gland due to damage to the hypothalamus or pituitary gland, leading to decreased production or release of ADH, or from defects in ADH receptors in the kidneys.

Renal tubular dysfunction occurs when the kidneys cannot respond to ADH appropriately, leading to decreased water reabsorption in the renal tubules. This can result from congenital defects in ADH receptors or acquired conditions such as electrolyte imbalances or medication-induced nephrogenic diabetes insipidus.

Risk Factors

Genetic Predispositions

Inherited or familial cases of DI can result from mutations in the AVPR2 or AQP2 genes that prevent the kidneys from responding to signals from ADH. Genetic counseling is crucial for individuals with a family history of DI to assess the risk of passing on genetic mutations and to understand potential inheritance patterns.

Environmental FactorsΒ 

Certain environmental conditions, such as hot weather or high altitude, can exacerbate symptoms of DI by increasing fluid loss through sweating and evaporation. Individuals with DI should take precautions to stay hydrated and avoid overheating.

Medications

Exposure to medications such as lithium, demeclocycline, or antiretroviral drugs can contribute to the development of DI. Additionally, exposure to toxins or heavy metals may impair kidney function, leading to nephrogenic DI.

Medical Conditions

Medical conditions that affect the hypothalamus, pituitary gland, or kidneys, such as brain tumors, head trauma, or chronic kidney disease, are associated with an increased risk of developing DI.

Diagnosis and Tests

History and Physical

A thorough medical history and physical examination to identify underlying conditions, medications, or lifestyle factors that may contribute to DI are key steps in diagnosis.Β 

Laboratory Testing

Laboratory testing to measure plasma and urine osmolality, or the concentration of solutes in blood and urine, helps to assess the kidney's ability to concentrate urine and overall hydration status.Β 

In DI, urine osmolality is typically low despite dehydration while plasma osmolality is typically elevated due to dehydration. In addition, serum electrolytes, especially sodium, may become imbalanced due to excessive urination in DI. Elevated sodium (hypernatremia) is common due to excessive water loss through urination without adequate replacement although low sodium can also occur if fluid intake is excessively high in an attempt to compensate for water loss.

Water Deprivation Test

A water deprivation test involves restricting fluid intake while monitoring urine output and osmolality. There is an inability to concentrate urine in response to water deprivation in central or nephrogenic DI, so urine remains dilute (urine osmolality <300 mOsm/kg) even after prolonged dehydration, confirming the diagnosis. Giving desmopressin results in a rise in urine osmolality (>800 mOsm/kg) in central DI but not in nephrogenic DI.Β 

Imaging Studies

Magnetic resonance imaging (MRI) or computed tomography (CT) imaging scans can identify structural abnormalities in the hypothalamus or pituitary gland, such as tumors or lesions, which may be causing DI.

Complications

Potential acute complications of DI include acute dehydration and electrolyte imbalances due to excessive urination, which can lead to symptoms such as weakness, dizziness, and confusion.Β 

Over time, chronic complications may arise from untreated or poorly controlled DI, including kidney damage, growth abnormalities in children, and cognitive impairments.Β 

Overall, DI can significantly impact the quality of life and contribute to psychological distress, affecting daily activities and social interactions.

Medical Treatments and Lifestyle Management Techniques

Advances in genetic research, imaging techniques, and biochemistry in the latter part of the 20th century and into the 21st century have further refined the understanding of the mechanisms underlying this condition, leading to additional treatment options for DI.Β 

Pharmacological Treatments

The medication desmopressin, a synthetic form of ADH, is the primary treatment for central DI, helping to reduce urine output and control symptoms.Β 

‍Medications such as thiazide diuretics or nonsteroidal anti-inflammatory drugs (NSAIDs) may be used in nephrogenic DI to reduce urine output by promoting sodium and water reabsorption in the kidneys.

Non-Pharmacological Treatments

Proper hydration strategies, such as carrying a water bottle and setting reminders to drink fluids, can help individuals with DI stay hydrated throughout the day. It is also important to monitor fluid intake and urine output to prevent dehydration.Β 

Dietary approaches, such as reducing salt (sodium) intake, can help prevent electrolyte imbalances in individuals with DI.

Psychological support and counseling may be beneficial for individuals dealing with the emotional impact of living with DI. In addition, participating in peer support groups can provide valuable emotional support and practical advice for managing DI.

Pregnancy and Diabetes Insipidus Management

Management of gestational diabetes insipidus involves careful monitoring of fluid balance and the use of desmopressin, a synthetic ADH analog that is not degraded by placental enzymes. Close monitoring by healthcare providers ensures maternal and fetal health are maintained throughout pregnancy.

Outlook / Prognosis

The prognosis for individuals with DI varies depending on the underlying cause, severity of symptoms, and effectiveness of treatment. With appropriate management and support, most individuals with DI can lead normal lives and maintain a good quality of life.Β 

Early diagnosis and treatment significantly improve outcomes, reducing the risk of complications such as dehydration and electrolyte imbalances. Other factors influencing prognosis include adherence to treatment, underlying health conditions, and access to healthcare resources for consistent monitoring and management.

[signup]

Key Takeaways

  • Diabetes insipidus (DI) is a condition characterized by excessive thirst and urination due to a deficiency of ADH or the inability of the kidneys to respond to ADH, resulting in impaired water regulation.
  • It can be classified into central DI (deficiency in antidiuretic hormone production), nephrogenic DI (kidney insensitivity to ADH), dipsogenic DI (abnormal thirst regulation), and gestational DI (occurs during pregnancy).
  • Causes include damage to the hypothalamus or pituitary gland, genetic factors, certain medications, and environmental factors.
  • Risk factors include a family history of DI, brain injuries, and exposure to medications like lithium.
  • Symptoms of DI include excessive thirst, frequent urination, dehydration, electrolyte imbalances, and growth abnormalities in children.
  • Complications may include kidney damage, cognitive impairment, and impact on quality of life.
  • Diagnosis involves medical history, physical examination, laboratory tests (urine and plasma osmolality, serum electrolytes), water deprivation test, and imaging studies (MRI, CT scan).
  • Pharmacological treatments include desmopressin to replace ADH in central DI and thiazide diuretics or NSAIDs to manage symptoms of excessive urination and electrolyte imbalance in nephrogenic DI.
  • Non-pharmacological treatments involve hydration strategies, dietary adjustments, and lifestyle modifications.
  • With proper management, most individuals with DI can lead normal lives and maintain a good quality of life.
  • Early diagnosis and treatment are crucial for improving outcomes and reducing the risk of complications.
  • Future research may focus on identifying novel therapeutic targets, improving diagnostic tools, and exploring personalized treatment approaches to optimize outcomes for individuals with DI.

Diabetes insipidus (DI) is associated with a deficiency of antidiuretic hormone (ADH) or an insensitivity to its effects. This can lead to challenges in conserving water, which may result in excessive thirst (polydipsia) and the excretion of large volumes of dilute urine (polyuria).Β 

Timely diagnosis and effective management of DI are important to help manage complications such as dehydration and electrolyte imbalances. This article aims to provide a comprehensive overview of DI, its symptoms, diagnosis, and management options to enhance awareness and support patient outcomes.

[signup]

What is Diabetes Insipidus?

When there is a deficiency in ADH or a reduced kidney response to ADH, the body may experience an imbalance in fluid regulation due to an inability to retain water effectively. This can result in excessive thirst (polydipsia) and the production of large volumes of dilute urine (polyuria) that characterizes diabetes insipidus. In DI, urine output is typically excessive, often exceeding 3 liters in 24 hours, with a very dilute concentration of osmolality less than 300 mOsm/kg.

Milestones in Understanding Diabetes Insipidus

The scientific understanding of DI has evolved significantly over several centuries since its first clinical description in the 18th century when patients were observed to have excessive thirst and urination without elevated blood glucose levels. In the early 20th century, researchers identified the hormone vasopressin (also known as ADH) and began to understand its important role in regulating water balance, bringing to light the intricacies of water balance in the body.Β 

Differentiation from Diabetes Mellitus

While the names sound similar, diabetes insipidus and diabetes mellitus involve different hormonal imbalances and causes. Diabetes derives from the Greek word siphon, referring to urine, or the fluid filtered out by the kidneys. While both conditions cause frequent urination and excessive thirst, these symptoms are caused by distinct underlying mechanisms.

Excessive dilute urine occurs in DI due to ADH insufficiency or resistance that causes impaired water retention. On the other hand, in diabetes mellitus, impaired insulin production results in impaired glucose metabolism and high blood sugar levels that contribute to excessive thirst and urination.Β 

Epidemiology of Diabetes Insipidus

DI is relatively rare, with an estimated prevalence of about 1 in 25,000 individuals. This condition occurs worldwide, with no specific geographic or ethnic predilection. There is no significant gender difference in the prevalence of DI, although some forms may show slight variations based on genetic factors.

DI can affect individuals of any age, but certain forms may have specific demographic patterns. DI arising from an issue with pituitary production of ADH (central DI) often arises in childhood or young adulthood, while DI occurring due to reduced kidney response to ADH (nephrogenic DI) can be congenital or acquired later in life.Β 

Causes of Diabetes Insipidus

DI results from either a deficiency in ADH production (central DI) or a reduced kidney response to ADH (nephrogenic DI). ​​

Central Diabetes Insipidus

Central DI, also referred to as arginine vasopressin (AVP)-deficiency, is the most common form of DI resulting from deficiency of the hormone AVP being released from the pituitary gland.Β 

Idiopathic Central DI

Idiopathic central diabetes insipidus occurs when the deficiency in ADH production occurs with no identifiable underlying condition or obvious damage to the hypothalamus or pituitary gland.

Secondary Central DI

When identifiable damage to the hypothalamus or pituitary gland, such as from pituitary tumors, head trauma, autoimmune attack, infections, or surgeries, results in DI this is classified as secondary central diabetes insipidus. This damage to the posterior pituitary gland impairs ADH production, leading to symptoms of DI.

Nephrogenic Diabetes Insipidus

The less common nephrogenic DI occurs when resistance develops in the kidneys, causing them not to respond sufficiently when stimulated with ADH.

Inherited Nephrogenic DI

Inherited or hereditary nephrogenic DI is a genetic disorder where the kidneys are unable to respond to ADH. Normally, ADH binds to its type-2 receptor (AVPR2 )in the kidneys' collecting duct, causing the exocytosis of the water channel aquaporin 2 (AQP2) at the apical membrane, allowing water to be reabsorbed. Inherited nephrogenic DI results due to mutations in the AVPR2 gene or AQP2 gene, affecting the receptors or channels necessary for water reabsorption.

Acquired Nephrogenic DI

Acquired nephrogenic DI occurs when external factors such as certain medications (e.g., lithium), chronic kidney disease, or electrolyte imbalances (e.g., hypercalcemia, hypokalemia) impair the kidneys' response to ADH.

Dipsogenic Diabetes Insipidus

Primary Dipsogenic DI

Primary dipsogenic DI is a type of primary polydipsia involving an abnormal increase in thirst and fluid intake. This condition is due to a malfunction in the thirst mechanism in the hypothalamus, leading to excessive drinking and subsequent dilution of urine.

Secondary Dipsogenic DI

Secondary dipsogenic DI occurs due to brain injuries, surgeries, or diseases affecting the hypothalamus or other areas that regulate thirst. These injuries cause abnormal stimulation of thirst, leading to excessive fluid intake and diluted urine.

Gestational Diabetes Insipidus

Gestational DI occurs during pregnancy, often in the third trimester, due to increased metabolism of ADH by placental enzymes (vasopressinase) and sometimes due to increased ADH clearance. It is usually transient during pregnancy.

Symptoms of Diabetes Insipidus

Due to the inability of the kidneys to concentrate urine adequately, common symptoms of DI may include:

In infants and children, symptoms of DI may manifest as irritability, poor feeding, failure to thrive, dehydration, dry skin, sunken fontanelles (soft spots on the head), lethargy, and delayed growth.Β 

Pathophysiology

ADH, also known as vasopressin, is a hormone released from the posterior pituitary gland that normally helps the kidneys retain water by concentrating urine.Β 

Dysfunction in the neurohypophyseal pathway involves impaired synthesis, release, or action of ADH in the hypothalamus or posterior pituitary gland due to damage to the hypothalamus or pituitary gland, leading to decreased production or release of ADH, or from defects in ADH receptors in the kidneys.

Renal tubular dysfunction occurs when the kidneys cannot respond to ADH appropriately, leading to decreased water reabsorption in the renal tubules. This can result from congenital defects in ADH receptors or acquired conditions such as electrolyte imbalances or medication-induced nephrogenic diabetes insipidus.

Risk Factors

Genetic Predispositions

Inherited or familial cases of DI can result from mutations in the AVPR2 or AQP2 genes that prevent the kidneys from responding to signals from ADH. Genetic counseling is crucial for individuals with a family history of DI to assess the risk of passing on genetic mutations and to understand potential inheritance patterns.

Environmental FactorsΒ 

Certain environmental conditions, such as hot weather or high altitude, can exacerbate symptoms of DI by increasing fluid loss through sweating and evaporation. Individuals with DI should take precautions to stay hydrated and avoid overheating.

Medications

Exposure to medications such as lithium, demeclocycline, or antiretroviral drugs can contribute to the development of DI. Additionally, exposure to toxins or heavy metals may impair kidney function, leading to nephrogenic DI.

Medical Conditions

Medical conditions that affect the hypothalamus, pituitary gland, or kidneys, such as brain tumors, head trauma, or chronic kidney disease, are associated with an increased risk of developing DI.

Diagnosis and Tests

History and Physical

A thorough medical history and physical examination to identify underlying conditions, medications, or lifestyle factors that may contribute to DI are key steps in diagnosis.Β 

Laboratory Testing

Laboratory testing to measure plasma and urine osmolality, or the concentration of solutes in blood and urine, helps to assess the kidney's ability to concentrate urine and overall hydration status.Β 

In DI, urine osmolality is typically low despite dehydration while plasma osmolality is typically elevated due to dehydration. In addition, serum electrolytes, especially sodium, may become imbalanced due to excessive urination in DI. Elevated sodium (hypernatremia) is common due to excessive water loss through urination without adequate replacement although low sodium can also occur if fluid intake is excessively high in an attempt to compensate for water loss.

Water Deprivation Test

A water deprivation test involves restricting fluid intake while monitoring urine output and osmolality. There is an inability to concentrate urine in response to water deprivation in central or nephrogenic DI, so urine remains dilute (urine osmolality <300 mOsm/kg) even after prolonged dehydration, confirming the diagnosis. Giving desmopressin results in a rise in urine osmolality (>800 mOsm/kg) in central DI but not in nephrogenic DI.Β 

Imaging Studies

Magnetic resonance imaging (MRI) or computed tomography (CT) imaging scans can identify structural abnormalities in the hypothalamus or pituitary gland, such as tumors or lesions, which may be associated with DI.

Complications

Potential acute complications of DI may include acute dehydration and electrolyte imbalances due to excessive urination, which can lead to symptoms such as weakness, dizziness, and confusion.Β 

Over time, chronic complications may arise from untreated or poorly managed DI, including kidney damage, growth abnormalities in children, and cognitive impairments.Β 

Overall, DI can significantly impact the quality of life and contribute to psychological distress, affecting daily activities and social interactions.

Medical Treatments and Lifestyle Management Techniques

Advances in genetic research, imaging techniques, and biochemistry in the latter part of the 20th century and into the 21st century have further refined the understanding of the mechanisms underlying this condition, leading to additional management options for DI.Β 

Pharmacological Treatments

The medication desmopressin, a synthetic form of ADH, is commonly used for central DI, helping to reduce urine output and manage symptoms.Β 

‍Medications such as thiazide diuretics or nonsteroidal anti-inflammatory drugs (NSAIDs) may be used in nephrogenic DI to help manage urine output by promoting sodium and water reabsorption in the kidneys.

Non-Pharmacological Treatments

Proper hydration strategies, such as carrying a water bottle and setting reminders to drink fluids, can help individuals with DI stay hydrated throughout the day. It is also important to monitor fluid intake and urine output to help prevent dehydration.Β 

Dietary approaches, such as reducing salt (sodium) intake, can help manage electrolyte imbalances in individuals with DI.

Psychological support and counseling may be beneficial for individuals dealing with the emotional impact of living with DI. In addition, participating in peer support groups can provide valuable emotional support and practical advice for managing DI.

Pregnancy and Diabetes Insipidus Management

Management of gestational diabetes insipidus involves careful monitoring of fluid balance and the use of desmopressin, a synthetic ADH analog that is not degraded by placental enzymes. Close monitoring by healthcare providers helps ensure maternal and fetal health are maintained throughout pregnancy.

Outlook / Prognosis

The prognosis for individuals with DI varies depending on the underlying cause, severity of symptoms, and effectiveness of management. With appropriate management and support, most individuals with DI can lead normal lives and maintain a good quality of life.Β 

Early diagnosis and management significantly improve outcomes, reducing the risk of complications such as dehydration and electrolyte imbalances. Other factors influencing prognosis include adherence to management plans, underlying health conditions, and access to healthcare resources for consistent monitoring and management.

[signup]

Key Takeaways

  • Diabetes insipidus (DI) is a condition characterized by excessive thirst and urination due to a deficiency of ADH or the inability of the kidneys to respond to ADH, resulting in impaired water regulation.
  • It can be classified into central DI (deficiency in antidiuretic hormone production), nephrogenic DI (kidney insensitivity to ADH), dipsogenic DI (abnormal thirst regulation), and gestational DI (occurs during pregnancy).
  • Causes include damage to the hypothalamus or pituitary gland, genetic factors, certain medications, and environmental factors.
  • Risk factors include a family history of DI, brain injuries, and exposure to medications like lithium.
  • Symptoms of DI include excessive thirst, frequent urination, dehydration, electrolyte imbalances, and growth abnormalities in children.
  • Complications may include kidney damage, cognitive impairment, and impact on quality of life.
  • Diagnosis involves medical history, physical examination, laboratory tests (urine and plasma osmolality, serum electrolytes), water deprivation test, and imaging studies (MRI, CT scan).
  • Pharmacological treatments include desmopressin to replace ADH in central DI and thiazide diuretics or NSAIDs to help manage symptoms of excessive urination and electrolyte imbalance in nephrogenic DI.
  • Non-pharmacological treatments involve hydration strategies, dietary adjustments, and lifestyle modifications.
  • With proper management, most individuals with DI can lead normal lives and maintain a good quality of life.
  • Early diagnosis and management are crucial for improving outcomes and reducing the risk of complications.
  • Future research may focus on identifying novel therapeutic targets, improving diagnostic tools, and exploring personalized management approaches to optimize outcomes for individuals with DI.
The information in this article is designed for educational purposes only and is not intended to be a substitute for informed medical advice or care. This information should not be used to diagnose or treat any health problems or illnesses without consulting a doctor. Consult with a health care practitioner before relying on any information in this article or on this website.

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Anderson, S. (2022, September 14). This is What Happens to Your Body When You are Dehydrated. Rupa Health. https://www.rupahealth.com/post/this-is-what-happens-to-your-body-when-you-are-dehydrated

Angelousi, A., Alexandraki, K. I., Mytareli, C., Grossman, A. B., & Kaltsas, G. (2023). New developments and concepts in the diagnosis and management of diabetes insipidus (AVP-deficiency and resistance). Journal of Neuroendocrinology, 35(1), e13233. https://doi.org/10.1111/jne.13233

Chandrashekhar, S., & Mishra, G. (2011). Management of diabetes insipidus in children. Indian Journal of Endocrinology and Metabolism, 15(7), 180. https://doi.org/10.4103/2230-8210.84858

Cleveland Clinic. (n.d.-a). Central Diabetes Insipidus (CDI): Symptoms, Diagnosis & Treatment. Cleveland Clinic. https://my.clevelandclinic.org/health/diseases/23515-central-diabetes-insipidus-cdi

Cleveland Clinic. (n.d.-b). Desmopressin (DDAVP) Tablets: Uses & Side Effects. Cleveland Clinic. https://my.clevelandclinic.org/health/drugs/19345-desmopressin-tablets

Cleveland Clinic. (n.d.-c). Nephrogenic Diabetes Insipidus: Symptoms & Treatment. Cleveland Clinic. https://my.clevelandclinic.org/health/diseases/24289-nephrogenic-diabetes-insipidus

Cleveland Clinic. (n.d.-d). What’s Your Baby’s Soft Spot Telling You? Cleveland Clinic. https://health.clevelandclinic.org/fontanelle-baby-soft-spot

Cleveland Clinic. (2017). Diabetes, Insipidus | Cleveland Clinic. Cleveland Clinic. https://my.clevelandclinic.org/health/diseases/16618-diabetes-insipidus

Cleveland Clinic. (2020, January 6). Nocturia. Cleveland Clinic. https://my.clevelandclinic.org/health/diseases/14510-nocturia

Cleveland Clinic. (2022a). Posterior Pituitary: What It Is & Function. Cleveland Clinic. https://my.clevelandclinic.org/health/body/23150-posterior-pituitary

Cleveland Clinic. (2022b, August 24). Polydipsia: Causes & Treatment. Cleveland Clinic. https://my.clevelandclinic.org/health/symptoms/24050-polydipsia

Cloyd, J. (2023a, July 5). Integrative Approaches to Managing High Blood Sugar: Specialty Testing, Lifestyle Modifications, and Natural Remedies. Rupa Health. https://www.rupahealth.com/post/integrative-approaches-to-managing-high-blood-sugar-testing-lifestyle-modifications-and-natural-remedies

Cloyd, J. (2023b, September 15). Top Labs To Run Bi-Annually On Your Patients Who Suffer From Kidney Disease. Rupa Health. https://www.rupahealth.com/post/top-labs-to-run-bi-annually-on-your-patients-who-suffer-from-kidney-disease

Cloyd, J. (2023c, September 28). Integrative Medicine Approach to Treating Hypotension. Rupa Health. https://www.rupahealth.com/post/integrative-medicine-approach-to-treating-hypotension

Cloyd, J. (2024, January 8). The Science of Hydration: How Water Intake Affects Overall Health. Rupa Health. https://www.rupahealth.com/post/the-science-of-hydration-how-water-intake-affects-overall-health

Cloyd, K. (2023, October 3). Functional Medicine Protocol for Autoimmune Diseases: Balancing the Immune System. Rupa Health. https://www.rupahealth.com/post/functional-medicine-protocol-for-autoimmune-diseases-balancing-the-immune-system

Cuzzo, B., Padala, S. A., & Lappin, S. L. (2020). Physiology, Vasopressin (Antidiuretic Hormone, ADH). PubMed; StatPearls Publishing. https://pubmed.ncbi.nlm.nih.gov/30252325/

DePorto, T. (2023, January 5). Signs you have an electrolyte imbalance & how to fix it. Rupa Health. https://www.rupahealth.com/post/electrolytes

Diorio, B. (2023, March 17). How to test for hypothalamic-pituitary-adrenal (HPA) axis dysfunction. Rupa Health. https://www.rupahealth.com/post/what-is-the-hypothalamic-pituitary-adrenal-hpa-axis

Eknoyan, G. (2010). A History of Diabetes Insipidus: Paving the Road to Internal Water Balance. American Journal of Kidney Diseases, 56(6), 1175–1183. https://doi.org/10.1053/j.ajkd.2010.08.002

Gerow, S. (2024, February 27). Neurological Health in Athletes: Preventing and Managing Concussions and Brain Injuries. Rupa Health. https://www.rupahealth.com/post/neurological-health-in-athletes-preventing-and-managing-concussions-and-brain-injuries

Greenan, S. (2021, December 14). Signs of toxic overload and how to properly detox. Rupa Health. https://www.rupahealth.com/post/a-functional-medicine-approach-to-detox

Hayek, A., & Ramirez, J. (1974). Demeclocycline-Induced Diabetes Insipidus. JAMA, 229(6), 676–677. https://doi.org/10.1001/jama.1974.03230440034026

Khakham, C. (2023, March 28). An integrative medicine approach to kidney disease. Rupa Health. https://www.rupahealth.com/post/an-integrative-medicine-approach-to-kidney-disease

Khanna, A. (2006). Acquired Nephrogenic Diabetes Insipidus. Seminars in Nephrology, 26(3), 244–248. https://doi.org/10.1016/j.semnephrol.2006.03.004

Knoers, N., & Lemmink, H. (1993). Hereditary Nephrogenic Diabetes Insipidus (M. P. Adam, H. H. Ardinger, R. A. Pagon, S. E. Wallace, L. J. Bean, K. W. Gripp, G. M. Mirzaa, & A. Amemiya, Eds.). PubMed; University of Washington, Seattle. https://www.ncbi.nlm.nih.gov/books/NBK1177/#:~:text=Hereditary%20nephrogenic%20diabetes%20insipidus%20(NDI

Kondo, T., Nakamura, M., Kitano, S., Kawashima, J., Matsumura, T., Ohba, T., Yamaguchi, M., Katabuchi, H., & Araki, E. (2018). The clinical course and pathophysiological investigation of adolescent gestational diabetes insipidus: a case report. BMC Endocrine Disorders, 18(1). https://doi.org/10.1186/s12902-018-0234-6

Leib, D. E., Zimmerman, C. A., & Knight, Z. A. (2016). Thirst. Current Biology, 26(24), R1260–R1265. https://doi.org/10.1016/j.cub.2016.11.019

Malone, S. (2023, March 8). What is Integrative Oncology and How Can it Help Your Cancer Journey? Rupa Health. https://www.rupahealth.com/post/what-is-integrative-oncology-and-how-can-it-help-your-cancer-journey

Malve, H., Kalra, S., Zargar, A., Jain, S., Sethi, B., Chowdhury, S., Singh, A., Thomas, N., Unnikrishnan, A., & Thakkar, P. (2016). Diabetes insipidus: The other diabetes. Indian Journal of Endocrinology and Metabolism, 20(1), 9. https://doi.org/10.4103/2230-8210.172273

Manelfe, C., & Louvet, J. P. (1979). Computed tomography in diabetes insipidus. Journal of Computer Assisted Tomography, 3(3), 309–316. https://doi.org/10.1097/00004728-197906000-00002

Marques, P., Gunawardana, K., & Grossman, A. (2015). Transient diabetes insipidus in pregnancy. Endocrinology, Diabetes & Metabolism Case Reports, 2015. https://doi.org/10.1530/edm-15-0078

MartΓ­n, D., Marcio JosΓ© ConcepciΓ³n-Zavaleta, Garxia, J., Alberto, E., SofΓ­a Pilar Ildefonso-Najarro, Rojas, J., & Luisa, C. (2021). Therapeutic challenge: Unusual coexistence of idiopathic central diabetes insipidus and diabetes mellitus in a male with vitiligo. DOAJ (DOAJ: Directory of Open Access Journals), 12(Suppl 2), S363–S367. https://doi.org/10.22088/cjim.12.0.363

McCarty, T. S., & Shah, A. D. (2020). Desmopressin. In www.ncbi.nlm.nih.gov. StatPearls Publishing. https://www.ncbi.nlm.nih.gov/books/NBK554582/

Mutter, C. M., Smith, T., Menze, O., Zakharia, M., & Nguyen, H. (2021). Diabetes Insipidus: Pathogenesis, Diagnosis, and Clinical Management. Cureus, 13(2). https://doi.org/10.7759/cureus.13523

National Library of Medicine. (n.d.-a). Osmolality blood test: MedlinePlus Medical Encyclopedia. Medlineplus.gov. https://medlineplus.gov/ency/article/003463.htm

National Library of Medicine. (n.d.-b). Urination - excessive amount: MedlinePlus Medical Encyclopedia. Medlineplus.gov. https://medlineplus.gov/ency/article/003146.htm

National Organization for Rare Diseases. (2015). Central Diabetes Insipidus - NORD (National Organization for Rare Disorders). NORD (National Organization for Rare Disorders); NORD. https://rarediseases.org/rare-diseases/central-diabetes-insipidus/

Orr, S. E., & Bridges, C. C. (2017). Chronic Kidney Disease and Exposure to Nephrotoxic Metals. International Journal of Molecular Sciences, 18(5), 1039. https://doi.org/10.3390/ijms18051039

Perkins, R. M., Yuan, C. M., & Welch, P. G. (2006). Dipsogenic diabetes insipidus: report of a novel treatment strategy and literature review. Clinical and Experimental Nephrology, 10(1), 63–67. https://doi.org/10.1007/s10157-005-0397-0

Preston, J. (2023, July 25). An integrative approach to prenatal care: Complementing conventional care with lab testing, nutrition, and other helpful therapies. Rupa Health. https://www.rupahealth.com/post/an-integrative-approach-to-prenatal-care-complementing-conventional-care-with-lab-testing-nutrition-and-other-helpful-therapies

Preston, J. (2024, February 20). How to Differentiate Common Pituitary Gland Disorders Using Lab Testing, Imaging, and Other Evaluations. Rupa Health. https://www.rupahealth.com/post/how-to-differentiate-common-pituitary-gland-disorders-using-lab-testing-imaging-and-other-evaluations

Priya, G., Kalra, S., Dasgupta, A., & Grewal, E. (2021). Diabetes Insipidus: A Pragmatic Approach to Management. Cureus, 13(1). https://doi.org/10.7759/cureus.12498

Sapra, A., & Bhandari, P. (2023, June 21). Diabetes. PubMed; StatPearls Publishing. https://www.ncbi.nlm.nih.gov/books/NBK551501/

Shin, J. H., Lee, H. K., Choi, C. G., Suh, D. C., Kim, C. J., Hong, S. K., & Na, D. G. (2001). MR Imaging of Central Diabetes Insipidus: A Pictorial Essay. Korean Journal of Radiology, 2(4), 222. https://doi.org/10.3348/kjr.2001.2.4.222

Singh, G. (2003). Latrogenic nephrogenic diabetes insipidus. AIDS, 17(9), 1418. https://journals.lww.com/aidsonline/citation/2003/06130/latrogenic_nephrogenic_diabetes_insipidus.30.aspx

Smith, A. E., & Badireddy, M. (2023, November 12). Failure To Thrive. PubMed; StatPearls Publishing. https://www.ncbi.nlm.nih.gov/books/NBK459287/

Sriram Gubbi, Fady Hannah-Shmouni, Koch, C. A., & Verbalis, J. G. (2019, February 10). Diagnostic Testing for Diabetes Insipidus. Nih.gov; MDText.com, Inc. https://www.ncbi.nlm.nih.gov/books/NBK537591/

Sweetnich, J. (2023a, March 15). Sodium 101: Lab Tests, Disorders, & How Much To Consume Daily. Rupa Health. https://www.rupahealth.com/post/sodium-101

Sweetnich, J. (2023b, March 28). Calcium 101: Testing, top foods, & supplements. Rupa Health. https://www.rupahealth.com/post/calcium-101-testing-top-foods-supplements

Sweetnich, J. (2023c, April 4). What is Potassium’s Role in The Body? Rupa Health. https://www.rupahealth.com/post/potassium-101

Sweetnich, J. (2023d, April 25). Complementary and Integrative Medicine Approaches to Type 2 Diabetes Management. Rupa Health. https://www.rupahealth.com/post/complementary-and-integrative-medicine-approaches-to-type-2-diabetes-management

Tasci, E. (2019). Lithium-Induced Nephrogenic Diabetes Insipidus Responsive to Desmopressin. Acta Endocrinologica (Bucharest), 15(2), 270–271. https://doi.org/10.4183/aeb.2019.270

Venkatesan, K., Chidambaram, K., Paulsamy, P., Ramaiah, R., Al-Qahtani, A., Venkatesan, K., Pappiya, E. M., Devidi, S., & Krishnaraju, K. (2021). A Subset of Primary Polydipsia, β€œDipsogneic Diabetes Insipidus”, in Apparently Healthy People Due to Excessive Water Intake: Not Enough Light to Illuminate the Dark Tunnel. Healthcare, 9(4), 406. https://doi.org/10.3390/healthcare9040406

Weinberg, J. L. (2024, April 10). ADH Hormone: Understanding Its Role in Body’s Fluid Balance. Rupa Health. https://www.rupahealth.com/post/adh-hormone-understanding-its-role-in-bodys-fluid-balance

Yoshimura, H. (2023, December 20). Functional Medicine for Mental Clarity: Combating Brain Fog Naturally. Rupa Health. https://www.rupahealth.com/post/functional-medicine-for-mental-clarity-combating-brain-fog-naturally

Young, B., & Verbalis, J. (2019, March 4). Diabetes insipidus. National Institute of Diabetes and Digestive and Kidney Diseases. https://www.niddk.nih.gov/health-information/kidney-disease/diabetes-insipidus

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