Diabetes insipidus
Formal Definition
A disorder of water balance characterized by excessive polyuria (urine output >3 L/day) and polydipsia, resulting from either inadequate ADH (vasopressin) secretion by the posterior pituitary (central diabetes insipidus) or inadequate renal response to ADH (nephrogenic diabetes insipidus); serum osmolality and sodium become elevated due to free water loss.
How It's Used on the Ward
"DI" — the patient is peeing out enormous volumes of dilute urine and can barely keep up with drinking; insipidus means "tasteless" (the urine is dilute, not sweet like in diabetes mellitus); the complaint is always "I drink everything and pee everything."
Example
""Post-craniopharyngioma resection patient now producing 6-8 L of urine/day, thirsty every hour, serum sodium 148 mEq/L, serum osmolality 302 mOsm/kg. Water deprivation test: urine osmolality remained at 85 mOsm/kg despite dehydration (max should reach 600+ if ADH working). After desmopressin: urine osmolality rose to 480 mOsm/kg. Diagnosis: central diabetes insipidus — surgically induced from posterior pituitary injury.""
Clinical Context
Central vs nephrogenic: central DI — ADH deficiency from pituitary/surgery/brain trauma/sarcoid Langerhans cell histiocytosis; nephrogenic DI — kidney resistance to ADH from lithium (most common drug cause), hypercalcemia, hypokalemia, chronic kidney disease. Diagnostic: water deprivation test with serial urine/serum osmolality, then desmopressin (DDAVP) challenge (central responds to DDAVP, nephrogenic does not). Copeptin: AVP precursor, elevated in nephrogenic. Treatment: central DI → intranasal or oral desmopressin (DDAVP); nephrogenic DI → address underlying cause, thiazide diuretics (paradoxical effect — cause mild volume depletion + increase proximal Na/H2O reabsorption), amiloride (specifically blocks lithium entry to collecting duct), low-sodium diet. Important: never restrict fluids in a patient with DI — risk of severe dehydration and hypernatremia.