Diabetes Insipidus - Diagnosis and Management Summary
Definition: ...

Diabetes Insipidus - Diagnosis and Management Summary

Definition: Polyuria (>3L/day) in setting of insufficient amount of ADH (central) or insufficient response to ADH (nephrogenic)


 • Central – hypothalamic or posterior pituitary damage by trauma, surgery, vascular (hemorrhage, infarction), neoplasm, infiltrative (sarcoidosis, histiocytosis), infection (meningitis, encephalitis), autoimmune, drugs (EtOH, phenytoin)

 • Nephrogenic – most frequently 2/2 drugs (lithium, cisplatin), hypercalcemia, or hereditary (children); also infiltrative (sarcoidosis, amyloidosis, MM), sickle cell

Diagnosis - Water restriction test:

 • Normal physiology: water restriction → ↑SOsm → ↑ADH → ↑UOsm

 • Check Na, SOsm, UOsm, UVol q2hr

     - If UOsm > 800 mEq/kg, stop test due to appropriate vasopressin response (dx: primary polydipsia)

     - If (1) SOsm > 295 mEq/kg, (2) Na > 145 mEq/L (adequate ADH stimulus) OR (3) UOsm stable on several checks despite ↑ SOsm (ADH response plateaued), administer vasopressin 4 mcg IV, then check UOsm, UVol q30min x 2hr

     - UOsm < 300 mEq/kg prior to vasopressin suggests complete DI

     - > 50% ↑ UOsm following vasopressin = central

     - < 50% ↑ UOsm following vasopressin = nephrogenic

     - UOsm 300 - 800 mEq/kg prior to vasopressin suggests partial DI (vs. primary polydipsia)


 • Correct hypernatremia (see Sodium Disorders). Allow patient to drink to thirst and if unable to drink, oral or nasogastric water is preferred to avoid rapid changes in serum sodium.

 • Central: first line = desmopressin (exogenous ADH); usually give intranasally (5mcg qHS + 5mcg 1-3x/day); additional meds (listed below) may be used as adjunctive therapy

 • Nephrogenic: if partial, may try desmopressin; if complete, use one of the meds listed below

 • Salt/protein restriction: low solute intake reduces thirst, thereby reducing free water intake

 • Adjunctive Meds:

    o HCTZ: volume depletion → increases proximal sodium/water reabsorption, decreasing distal sodium delivery (where ADH acts)

    o Amiloride: mechanism similar to HCTZ; also beneficial in lithium-induced nephrogenic DI by blocking entry of lithium across ENaC into collecting tubule cells, thereby preventing toxicity

    o NSAIDs: enhance renal response to ADH (prostaglandins antagonize ADH)

    o Chlorpropamide: enhances renal response to ADH

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