Is this patient's presentation of hyperosmolality with inability to concentrate urine, serum osmolality of 300, urine osmolality of 170, and serum sodium of 143 consistent with central diabetes insipidus?

Diagnosis: Diabetes Insipidus

Yes, this presentation is consistent with diabetes insipidus—the combination of serum osmolality 300 mOsm/kg, urine osmolality 170 mOsm/kg, and serum sodium 143 mEq/L represents the pathognomonic triad of hyperosmolality with inappropriately dilute urine that confirms the diagnosis. 1

Diagnostic Confirmation

Your patient's laboratory values definitively establish diabetes insipidus:

• Serum osmolality 300 mOsm/kg (elevated, indicating hyperosmolar state) 1
• Urine osmolality 170 mOsm/kg (inappropriately dilute—should be >600 mOsm/kg with this degree of serum hyperosmolality) 2, 1
• Serum sodium 143 mEq/L (high-normal, consistent with DI) 1
• Urine sodium 39 mEq/L (not diagnostic but consistent with ongoing water loss) 2

The physiologic impossibility of producing dilute urine (osmolality <200 mOsm/kg) in the presence of elevated serum osmolality confirms impaired urinary concentration, which is the hallmark of diabetes insipidus. 3

Distinguishing Central vs. Nephrogenic DI

The next critical step is plasma copeptin measurement to differentiate between central and nephrogenic diabetes insipidus:

• Copeptin >21.4 pmol/L indicates nephrogenic DI (kidneys insensitive to ADH) 1, 3
• Copeptin <21.4 pmol/L indicates central DI (ADH deficiency) or requires additional stimulation testing 1

If copeptin is unavailable, perform a desmopressin trial: response with increased urine osmolality confirms central DI, while no response indicates nephrogenic DI. 1

Additional Required Workup

Immediate investigations needed:

• 24-hour urine volume to quantify polyuria (expect >3 L/day in adults) 1, 3
• Serum creatinine and electrolytes (potassium, calcium, chloride) to assess renal function and exclude other causes 1
• Blood glucose to definitively exclude diabetes mellitus (fasting glucose ≥126 mg/dL or random ≥200 mg/dL would indicate DM, not DI) 1
• Pituitary MRI with dedicated sella sequences if central DI is confirmed, as metastatic disease is the most common cause 1

Critical Management Principles

Regardless of DI subtype, ensure free access to water at all times—this is life-saving. Patients with DI depend entirely on thirst-driven fluid intake to prevent life-threatening hypernatremic dehydration. 1, 3, 4

If IV hydration is required:

• Use 5% dextrose in water, NOT normal saline (which would worsen hypernatremia given the kidneys cannot concentrate urine) 3
• Start at physiologic maintenance rates: 25-30 mL/kg/24h in adults 3

Treatment Based on Final Diagnosis

For Central DI:

• Desmopressin is the treatment of choice (2-4 mcg subcutaneously/IV initially, or intranasal/oral formulations) 1
• Monitor serum sodium within 7 days and at 1 month after starting treatment—hyponatremia is the main complication 1

For Nephrogenic DI:

• Combination therapy: thiazide diuretics + NSAIDs (can reduce diuresis by up to 50%) 5, 1
• Dietary modifications: low-salt diet (≤6 g/day) and protein restriction (<1 g/kg/day) 1
• Genetic testing with multigene panel (AVPR2, AQP2, AVP genes) is recommended even in adults 1

Common Pitfalls to Avoid

Do not confuse with SIADH, which presents with the opposite pattern: hyponatremia (sodium <134 mEq/L), low serum osmolality (<275 mOsm/kg), and inappropriately HIGH urine osmolality (>500 mOsm/kg). 2

Do not confuse with diabetes mellitus, which causes polyuria through osmotic diuresis from glucosuria, not from ADH deficiency—DM would show elevated blood glucose and high urine osmolality from glucose. 1

Watch for atypical presentations: patients with impaired thirst (adipsic DI) may present with severe hypernatremia without polydipsia, making diagnosis particularly challenging. 6, 4