Diabetes insipidus Flashcards
What is diabetic inspidius?
metabolic disorder characterised by an absolute or relative inability to concentrate urine, resulting in the production of large quantities of dilute urine.
due to the patient’s inability to make ADH or respond to ADH. This leads to polydipsia, polyuria, and hypotonic urine.
Epidemiology of DI
- DI is uncommon, although the exact prevalence is difficult to estimate.
- There are no differences in prevalence between sexes or among ethnic groups.
- Inherited causes for both central and nephrogenic DI account for less than 10% of all cases.
Nephrogenic (Kidney) aetiology/causes of DI
- Drugs e.g. Lithium, Demeclocycline
- Genetic - AVR2 gene X chromosome
- Intrinsic kidney disease
- Post-obstructive uropathy - urine can’t flow due to obstruction and so refluxes back into kidney
- Electrolyte imbalances - mainly hypokalaemia and hypercalcaemia
Cranial aetiology/ causes of DI
Idiopathic
Brain tumours
Head injuries
Infections - meningitis, encephalitis, TB
Congenital defects in ADH gene
RF for DI
- Pituitary surgery
- Craniopharyngioma
- Brain injury
- Congenital pituitary abnormalities
- Medication e.g. lithium
- Autoimmune disease - some cases linked to antibodies against ADH secreting cells
- Family history
- CNS infections
- Pregnancy
Central DI
results from any condition that impairs the production, transportation, or release of ADH.
Nephrogenic DI
results from conditions that impair the renal collecting ducts’ ability to respond to ADH.
Pathophysiology of DI
Both central and nephrogenic DI are characterised by impaired renal water re-absorption, resulting in the production of excessive, hypotonic (dilute) urine (polyuria).
This is accompanied by significant thirst and increased drinking (polydipsia), as central osmo-sensing and peripheral baro-sensing drive central thirst and thirst-dependent behaviours to maintain circulating volume and osmolar status.
Signs of DI
- Postural hypotension
- Hypernatraemia
Symptoms of DI
- Polyuria
- Polydipsia
- Dehydration
1st line investigation for DI
- U&E - hypernatraemia found
- Serum glucose - exclude DM
- Urine osmolality - low urine osmolality found
-
Serum osmolality - high serum osmolality found
Water deprivation test
What is the gold standard investigation?
Water deprivation test (desmopressin suppression test)
What is the water deprivation test?
avoid taking fluid or foods 8 hrs before test. Then urine osmolality is measured followed by giving desmopressin. 8 hrs later urine osmolality is measured again. Allows us to differentiate between cranial and nephrogenic diabetes insipidus
Differential diagnosis for DI
- Primary polydipsia - normal ADH, but excessive thirst and excessive urine production. In the water deprivation test, patient’s with primary polydipsia will already have high urine osmolality prior to desmopressin administration.
- Diabetes mellitus - due to polyuria and polydipsia
- Hypercalcaemia
1st line management for Cranial DI
- Correct underlying cause
- Mild cases can be managed conservatively e.g. low sodium diet
-
Desmopressin
- Used in cranial DI to replace ADH
- Can be used in nephrogenic DI at very high doses. This needs monitoring
