Diabetes Insipidus

Posted by e-Medical PPT Tuesday, September 20, 2011
Diabetes Insipidus: Pathogenesis
Inability to concentrate urine

Central
ADH deficiency from hypothalamo-neurohypophyseal damage or atrophy, ADH mutations
Nephrogenic
 Renal inability to respond to ADH secondary to disturbance of corticomedullary osmotic gradient, defect of ADH-cAMP system, or osmotic diuresis.

Psychogenic polydipsia
 physiologic ADH inhibition

Presentation
Polyuria > 3 liters in 24 hrs
Sudden onset more typical of central DI
Nocturia
Polydipsia
Dilute urine w/ SG < 1.010, urine osm < 200
Serum Na > 150 rare if free access to H20
Dehydration when access to water limited
May have family history

Central Diabetes Insipidus: Etiology
Brain tumors
Lung cancer, leukemia, lymphoma most common
Head trauma
Post-neurosurgery
Idiopathic – 30-50%
Pituitary atrophy, possible autoimmune
Congenital
Mutations of ADH gene, usually autosomal dominant
Infiltrative diseases, such as Histiocytosis X or sarcoidosis
HIE

Nephrogenic DI: Etiology
Acquired
Drugs: lithium, amphotericin, gentamicin, loop diuretics
Electrolyte disorders: hypercalcemia, hypokalemia
Renal dz: obstructive uropathy, CRF, PCKD, post-transplant, pyelonephritis
Systemic processes: sarcoid, amyloid, multiple myeloma, sickle cell disease, pregnancy
Congenital – rare
Present in 1st week of life
V2 ADH receptor defect – X-linked recessive
AQP2 water channel defect – will respond to ADH

Lithium and the kidney
Lithium use can cause RTA, nephrotic syndrome, interstitial nephritis, and is the most common cause of acquired nephrogenic DI. 

Lithium-induced DI
Lithium accumulates in collecting tubule cells, interfering with several water/urea channels, impairing urinary concentrating ability.
Up to 55% pf pts develop after long-term lithium use
May lead to hypovolemia and impaired lithium excretion, which then increase lithium blood levels and precipitate toxicity.

Treatment
Prevention with amiloride therapy – closes Na channels and prevents lithium accumulation in tubular cells.
lithium cessation or careful blood level monitoring plus amiloride
Reversibility depends on severity of concentrating defect

Diagnosis
Initial labs:
Na, Cl, Ca, Glu, BUN, Cr, serum osmolality
24 hour urine collection to quantify polyuria & estimate osmolar excretion rate
SG from 1st morning void
Urine osmolality, Na
Should have polyuria, low urine SG and osm in the context of normal to high serum Na and osm.
Distinguish from other causes of polyuria
Solute diuresis (i.e. DM) – urine-to-plasma osm ratio >0.7
Renal disease – elevated creatinine
Small volume frequency (i.e. cystitis) – not true polyuria

Long-term effects
Life-threatening dehydration
Can occur when free water access limited (i.e. infancy, LOC, anesthesia)

Mental retardation
Secondary to hypernatremic dehydration, encephalopathy, seizures
Very uncommon now 

Renal
Nonobstructive functional hydronephrosis – monitor with renal US.
CRI secondary to dehydration induced glomerular thromboemboli.

Post-neurosurgical DI usually resolves, but may become permanent if still present beyond a few weeks.

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