Diabetes Insipidus
last authored: October 2009, David LaPierre
Introduction
Diabetes insipidus (DI) results from an inability of the kidneys to concentrate urine.
The Case of...
a simple case introducing clincial presentation and calling for a differential diagnosis. To get students thinking.
Causes and Risk Factors
Central DI results from decreased ADH production in the brain. Causes include:
- congenital
- trauma
- surgery
- radiation
- neoplasm
- meningitis
Nephrogenic DI results from:
- genetic (X-linked) condition affecting kidneys
- drug-induced (lithium)
Pathophysiology
Central DI is caused by a loss of ADH-secreting cells from the posterior pituitary.
Signs and Symptoms
- history
- physical exam
History
Central DI presents with polyuria, polydipsia, and enuresis
progressive dehydration
Nephrogenic DI leads to polyuria, failure to thrive, vomiting, and dehydration leading to hypernatremia.
Physical Exam
Investigations
- lab investigations
- diagnostic imaging
Lab Investigations
Fasting serum osmolality above 650 excludes DI, and if 24-h urine volume is below 2.5L and serum Na is normal, DI is unlikely.
Serum
- high osmolality
- hypernatremia
Urinalysis shows a dilute urine (SG <1.010) and low urine osmolality.
ADH administration test leading to >50% change in urine osmolality suggests central cause.
Diagnostic Imaging
Differential Diagnosis
Cerebral salt wasting (high serum Na, ++ hypovolemic)
Treatments
Treatment is aimed at correcting the free water deficit.
Central DI is managed with DDAVP, given intranasally, SC, or PO.
Nephrogenic DI is managed with a low solute diet or with thiazide diuretics to excrete salt.
- IV fluids
- Na restriction
Consequences and Course
Additional Resources
Topic Development
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