Diabetes insipidus overview: Difference between revisions
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==Historical Perspective== | ==Historical Perspective== | ||
The history of Diabetes Insipidus dates as far back as the early 1670s when Thomas Willis noted that there was a difference in the taste of urine produced by different patients who presented with polyuria and polydipsia and this marked the beginning of the research into the difference between the popularly known diabetes mellitus and diabetes insipidus. | |||
==Classification== | ==Classification== | ||
Diabetes Insipidus can be classified into central and nephrogenic diabetes insipidus based on the response of the body to administration of desmopressin (DDAVP). It can also be classified based on the | Diabetes Insipidus can be classified into central and nephrogenic diabetes insipidus based on the response of the body to administration of desmopressin (DDAVP). It can also be classified based on the level of desmopressin (DDAVP) and the levels of hypo- or hypernatremia in the body. | ||
==Pathophysiology== | ==Pathophysiology== | ||
Revision as of 13:05, 14 July 2017
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Diabetes insipidus (DI) is a syndrome characterized by the excretion of abnormally large volumes of dilute urine. It can be classified into 4 fundamentally different types that must be distinguished for safe and effective management. They are: (1) Central DI also called neurogenic DI, due to inadequate production and secretion of antidiuretic hormone, arginine-vasopressin (AVP), (2) Nephrogenic DI due to renal insensitivity to the antidiuretic effect of AVP (3) Primary polydipsia also known as psychogenic DI, due to suppression of arginine vasopressin secretion by excessive fluid intake and (4)Gestational DI due to degradation of arginine vasopressin by an enzyme made in placenta. Patients with DI typically present with excessive day and nighttime urination, excessive drinking of fluids in order to compensate for the lost fluids in urine which may lead to electrolyte imbalances such as hypo- or hypernatremia. The causes of Diabetes insipidus are unique to the type of the diabetes insipidus caused, and the treatment should be targeted at understanding the underlying cause of the disease.
Historical Perspective
The history of Diabetes Insipidus dates as far back as the early 1670s when Thomas Willis noted that there was a difference in the taste of urine produced by different patients who presented with polyuria and polydipsia and this marked the beginning of the research into the difference between the popularly known diabetes mellitus and diabetes insipidus.
Classification
Diabetes Insipidus can be classified into central and nephrogenic diabetes insipidus based on the response of the body to administration of desmopressin (DDAVP). It can also be classified based on the level of desmopressin (DDAVP) and the levels of hypo- or hypernatremia in the body.
Pathophysiology
Causes
Diabetes insipidus is caused by a variety of factors. The causes for each subtype of diabetes insipidus is classically different. It is important to identify these underlying causes of the various forms in order to appropriately diagnose and treat each type.
Differentiating Diabetes insipidus other Diseases
Diabetes insipidus must be differentiated from other diseases that cause polyuria which is defined as a urine output exceeding 3 L/day in adults and 2 L/m2 in children, increased frequency or nocturia and polydipsia. It is important to know that levels of hypo or hypernatremia is not sufficient to describe the underlying cause of diabetes insipidus.
Epidemiology and Demographics
The prevalence of diabetes insipidus is estimated to be 3:100,000. The prevalence and incidence of both central and nephrogenic DI does not vary by gender. Similarly, no significant racial predilection in prevalence among ethnic groups have been found.
With both central and nephrogenic DI, inherited causes account for approximately 1-2% of all cases. An incidence of about 1 in 20 million births for nephrogenic DI caused by AQP2 mutations has been documented.[1]
Risk Factors
Screening
According to the USPSTF screening for diabetes insipidus is not recommended.
Natural History, Complications and Prognosis
Diagnosis
History and Symptoms
Physical Examination
Laboratory Findings
Electrocardiogram
Chest X Ray
CT
MRI
Echocardiography or Ultrasound
Other Imaging Findings
Other Diagnostic Studies
Treatment
Surgery
Medical Therapy
Primary Prevention
Secondary Prevention
Cost-Effectiveness of Therapy
Future or Investigational Therapies
Case Studies
Case #1
References
- ↑ Verkman AS (2012). "Aquaporins in clinical medicine". Annu. Rev. Med. 63: 303–16. doi:10.1146/annurev-med-043010-193843. PMC 3319404. PMID 22248325.