Is diabetes insipidus evident in these laboratory results?

Laboratory Findings Consistent with Diabetes Insipidus

Yes, these laboratory results are diagnostic of diabetes insipidus. A urine osmolality of 170 mOsm/kg combined with a serum osmolality of 300 mOsm/kg represents inappropriately diluted urine in the setting of elevated serum osmolality, which is pathognomonic for diabetes insipidus 1.

Key Diagnostic Features Present

The combination of inappropriately diluted urine (urine osmolality <200 mOsm/kg H₂O) with high-normal or elevated serum sodium is pathognomonic for diabetes insipidus 1, 2. Specifically:

• Urine osmolality of 170 mOsm/kg is inappropriately low given the serum osmolality of 300 mOsm/kg, confirming the diagnosis 1
• The serum osmolality of 300 mOsm/kg is at the high-normal to elevated range, indicating the body is attempting to concentrate but the kidneys are failing to respond appropriately 1
• This pattern excludes primary polydipsia, which would typically present with lower serum sodium and osmolality due to excessive water intake 1

Next Steps to Determine DI Type

You must now distinguish between central diabetes insipidus (vasopressin deficiency) and nephrogenic diabetes insipidus (vasopressin resistance) 1, 2:

Plasma Copeptin Measurement (Preferred)

• Baseline plasma copeptin levels above 21.4 pmol/L are diagnostic for nephrogenic DI in adults, indicating significantly elevated ADH levels despite lack of renal response 1, 2
• Low or absent copeptin suggests central DI, indicating inadequate vasopressin production 2

DDAVP Challenge Test (Alternative)

• Administration of desmopressin with subsequent increase in urine osmolality and decreased urine volume confirms central DI 1, 3
• Lack of response to desmopressin indicates nephrogenic DI 1

Essential Additional Workup

For Central DI

• MRI of the sella turcica with contrast using high-resolution pituitary protocols is mandatory to evaluate for hypothalamic-pituitary pathology including tumors, infiltrative processes, or structural abnormalities 1, 3, 2
• Look for absence of the typical T1 hyperintensity of normal neurosecretory granules in the posterior pituitary, which may indicate central DI 3, 2

For Nephrogenic DI

• Genetic testing of AVPR2 and AQP2 genes is recommended, particularly if symptoms began in early childhood, as ~90% of nephrogenic DI cases are X-linked due to AVPR2 mutations 1, 2
• Kidney ultrasound should be performed to evaluate for urinary tract dilation and bladder dysfunction from chronic polyuria 2

Critical Management Considerations

Before initiating any treatment, confirm that serum sodium is normal and establish the specific type of DI 1, 2:

• For central DI: Desmopressin is the treatment of choice, starting at 2-4 mcg daily as one or two divided doses by subcutaneous or IV injection 1
• For nephrogenic DI: Thiazide diuretics combined with prostaglandin synthesis inhibitors (NSAIDs) are recommended, along with dietary salt restriction (≤6 g/day) and protein restriction (<1 g/kg/day) 2, 4

Important Caveat

• Fluid restriction must be initiated during desmopressin treatment to prevent hyponatremia, particularly in children and elderly patients who are at higher risk 1, 5