2.1
Diabetes Insipidus, or DI, is a syndrome that features excessive urination, known as polyuria, and intense thirst, called polydipsia.
It develops either due to a deficiency of the antidiuretic hormone ADH or because the kidneys cannot effectively respond to ADH.
In the absence of ADH, the kidneys excrete 10 to 20 liters of dilute urine daily, compared to the normal 1 to 2 liters of concentrated urine.
Clinically, DI presents with frequent urination even during dehydration, marked nocturia in adults, and enuresis in children.
Thirst is a prominent symptom, and when fluid intake does not match urinary loss, dehydration can develop.
There are three main types of DI.
Central DI results from reduced ADH production, often due to brain injury or intracranial tumors.
Nephrogenic DI results from the kidneys' inability to respond appropriately to ADH, often associated with chronic kidney disease or certain drugs like lithium carbonate.
Gestational DI can develop during pregnancy due to an excess production of placental vasopressinase, which breaks down ADH.
Definition
Diabetes insipidus is a disorder marked by the production of large amounts of dilute urine because of impaired vasopressin production, release, or kidney response. The lack of effective vasopressin action limits water reabsorption in the renal collecting ducts, which leads to excessive urinary water loss and intense thirst.
Clinical Presentation
Individuals with diabetes insipidus report persistent thirst and very high urine output. In severe cases, fluid intake can reach up to 20 liters per day. Adults often describe frequent nighttime urination, while children may present with bed-wetting. If fluid intake does not match the degree of urinary loss, rapid dehydration can develop. This may cause high serum sodium levels and neurologic changes such as irritability, confusion, seizures, or coma.
Etiology and Types
Central Diabetes Insipidus
Central diabetes insipidus happens when vasopressin synthesis or release decreases. This usually follows injury to the hypothalamus or posterior pituitary. Common causes include head trauma, neurosurgical procedures, tumors such as craniopharyngiomas, infections, autoimmune disorders, or inherited genetic variants.
Nephrogenic Diabetes Insipidus
Nephrogenic diabetes insipidus happens when the kidneys fail to respond to vasopressin. It can be present from birth because of mutations affecting vasopressin receptors or aquaporin channels. It can also appear later due to chronic kidney disease, lithium exposure, kidney infections like pyelonephritis, or electrolyte disturbances, including high calcium or low potassium levels.
Gestational Diabetes Insipidus
Gestational diabetes insipidus develops during pregnancy. The placenta produces vasopressinase, an enzyme that breaks down circulating vasopressin and lowers its effectiveness.
Primary Polydipsia
Primary polydipsia, also called dipsogenic diabetes insipidus, happens when fluid intake becomes excessively high. This pattern may relate to psychiatric conditions or hypothalamic dysfunction and suppresses vasopressin release.
Diabetes Insipidus, or DI, is a syndrome that features excessive urination, known as polyuria, and intense thirst, called polydipsia.
It develops either due to a deficiency of the antidiuretic hormone ADH or because the kidneys cannot effectively respond to ADH.
In the absence of ADH, the kidneys excrete 10 to 20 liters of dilute urine daily, compared to the normal 1 to 2 liters of concentrated urine.
Clinically, DI presents with frequent urination even during dehydration, marked nocturia in adults, and enuresis in children.
Thirst is a prominent symptom, and when fluid intake does not match urinary loss, dehydration can develop.
There are three main types of DI.
Central DI results from reduced ADH production, often due to brain injury or intracranial tumors.
Nephrogenic DI results from the kidneys' inability to respond appropriately to ADH, often associated with chronic kidney disease or certain drugs like lithium carbonate.
Gestational DI can develop during pregnancy due to an excess production of placental vasopressinase, which breaks down ADH.
From Chapter 2:
Now Playing
Endocrine Disorders
1.1K Views
Endocrine Disorders
514 Views
Endocrine Disorders
189 Views
Endocrine Disorders
185 Views
Endocrine Disorders
145 Views
Endocrine Disorders
176 Views
Endocrine Disorders
147 Views
Endocrine Disorders
183 Views
Endocrine Disorders
195 Views
Endocrine Disorders
169 Views
Endocrine Disorders
225 Views
Endocrine Disorders
181 Views
Endocrine Disorders
226 Views
Endocrine Disorders
137 Views
Endocrine Disorders
135 Views
See More