Diagnosis: Central Diabetes Insipidus
This patient has central diabetes insipidus (CDI), characterized by inappropriately low ADH (<0.8 pg/mL) in the setting of high-normal serum sodium (143 mEq/L) and serum osmolality (295 mOsm/kg), with inappropriately dilute urine (osmolality 220 mOsm/kg) and high urine output (1300 mL). 1, 2
Diagnostic Reasoning
The key diagnostic feature is the dissociation between elevated serum osmolality and suppressed ADH with dilute urine. 1
Serum osmolality of 295 mOsm/kg should stimulate ADH release, but ADH remains suppressed at <0.8 pg/mL (reference range 0.0-4.7), indicating failure of ADH secretion. 1
The urine osmolality of 220 mOsm/kg is inappropriately low for the serum osmolality of 295 mOsm/kg—in CDI, the kidneys cannot concentrate urine despite physiologic need. 1, 2
Urine output of 1300 mL with dilute urine confirms polyuria, though this is relatively mild CDI (severe cases produce >3-4 L/day). 2
The low urine sodium (26 mEq/L random, 34 mEq/24hr) and low BUN (9 mg/dL) suggest adequate volume status without significant volume depletion. 1
Differential Diagnosis Considerations
This is NOT nephrogenic diabetes insipidus because ADH is suppressed rather than elevated. 1 In nephrogenic DI, ADH levels would be normal or elevated as the hypothalamus attempts to compensate for renal resistance. 1
This is NOT primary polydipsia because serum osmolality and sodium are high-normal rather than low-normal. 1 Primary polydipsia causes dilutional hyponatremia with plasma osmolality below 280 mOsm/kg. 1
This is NOT SIADH, which presents with hyponatremia, not hypernatremia, and elevated rather than suppressed ADH. 3
Treatment Algorithm
First-Line Treatment: Desmopressin (DDAVP)
Desmopressin is the definitive treatment for central diabetes insipidus, replacing the deficient ADH. 4, 2
Start with desmopressin 0.1-0.2 mg orally at bedtime (one tablet), then titrate upward to 0.2-0.6 mg daily in divided doses based on urine output and serum sodium. 4
The goal is to reduce urine output to normal range (1-2 L/day) and maintain serum sodium between 135-145 mEq/L. 4
Monitor serum sodium and osmolality closely during initiation—at minimum once within the first week, then periodically. 4
Critical Monitoring Parameters
Monitor the following to prevent water intoxication and hyponatremia: 4
- Daily urine output and specific gravity initially, then as clinically indicated 4
- Serum sodium and osmolality at least once early in treatment, then with any intercurrent illness or unexplained symptoms 4
- Body weight daily initially to detect fluid retention 4
Dose Titration Strategy
Increase desmopressin dose incrementally (by 0.1 mg) every 3-7 days until urine output normalizes and serum sodium stabilizes. 4
Most patients require 0.2-0.6 mg daily in 1-2 divided doses. 4
Duration of action is 10-12 hours, so twice-daily dosing may be needed for 24-hour coverage. 4
Common Pitfalls to Avoid
Do NOT restrict fluid intake excessively—patients should drink to thirst, as desmopressin will prevent excessive urination. 2 Forced fluid restriction with desmopressin can cause dangerous hyponatremia. 4
Watch for water intoxication, especially during intercurrent illnesses that affect hydration or drug absorption. 4 Symptoms include headache, nausea, confusion, and seizures from hyponatremia. 4
Obtain serum sodium if the patient develops unexplained headache, abdominal discomfort, nausea, or neurologic symptoms. 4 These may indicate hyponatremia from excessive desmopressin effect. 4
Alternative Considerations
If this patient has partial CDI (some residual ADH secretion), lower doses of desmopressin may suffice. 2 The relatively mild polyuria (1300 mL) and borderline serum sodium suggest partial rather than complete ADH deficiency. 2
Investigate the underlying cause of CDI—obtain MRI of the pituitary/hypothalamus to evaluate for tumor, infiltrative disease, or structural abnormality. 2 CDI in adults is often secondary to pituitary surgery, trauma, or tumor. 2