What are the clinical signs of diabetes insipidus?

Clinical Signs of Diabetes Insipidus

The pathognomonic triad of diabetes insipidus consists of polyuria with inappropriately dilute urine (osmolality <200 mOsm/kg H₂O), polydipsia, and high-normal or elevated serum sodium. 1

Cardinal Clinical Features in Adults

• Polydipsia is the predominant symptom at diagnosis in adults, often with patients consuming several liters of fluid daily driven by an intact and highly sensitive thirst mechanism 1
• Polyuria exceeding 3 liters per 24 hours with urine that remains dilute despite attempts to reduce fluid intake 2
• Nocturia and nocturnal enuresis, with approximately 46% of patients developing urological complications including "bed flooding" 2
• Normal serum sodium levels at steady state when free water access is available, as the intact thirst mechanism drives adequate fluid replacement 2

Distinct Presentation in Infants and Children

• Feeding difficulties, failure to thrive, vomiting, and hypernatremic dehydration are the common presentations in pediatric patients 1
• "Greedy" drinking behavior followed by vomiting, particularly in infants, thought to reflect gastroesophageal reflux exacerbated by large fluid volumes 2
• Growth failure and constipation when fluid access is inadequate 2, 3
• Infants and toddlers cannot clearly express thirst, making recognition more challenging and requiring vigilant caregiver observation 2

Critical Biochemical Hallmarks

• Urine osmolality definitively <200 mOsm/kg H₂O in the presence of serum hyperosmolality or high-normal serum sodium confirms the diagnosis 1, 2
• Urine specific gravity <1.005 (equivalent to osmolality <200 mOsm/kg) 2
• Serum sodium >145 mEq/L when water access is restricted, indicating life-threatening hypernatremic dehydration 2
• The combination of dilute urine with elevated or high-normal serum sodium distinguishes DI from other causes of polyuria 1

Physical Examination Findings

• Signs of dehydration including poor skin turgor, dry mucous membranes, and weight loss when fluid intake cannot match urinary losses 4, 5
• Neurologic symptoms and encephalopathy in severe, uncompensated cases with marked dehydration 5
• Normal blood glucose levels, distinguishing DI from diabetes mellitus which causes polyuria through osmotic diuresis from glucosuria 1, 2

Important Clinical Pitfalls

• Many patients maintain normal serum sodium at baseline because their thirst mechanism is intact and drives compensatory fluid intake—do not be falsely reassured by normal sodium 2
• Hypernatremia only develops when water access is restricted or the patient cannot communicate thirst (infants, cognitively impaired patients) 2, 3
• Patients with cognitive impairment cannot self-regulate fluid intake and require proactive water offering with close monitoring of weight, fluid balance, and biochemistry 2
• Never restrict water access in suspected DI—this is a life-threatening error leading to severe hypernatremic dehydration 2, 3

Differentiating Features from Other Conditions

• Unlike diabetes mellitus, DI patients have normal blood glucose and no glucosuria; diabetes mellitus causes polyuria through osmotic diuresis with high urine osmolality from glucose 2
• Unlike SIADH, DI presents with high-normal or elevated serum sodium and dilute urine, whereas SIADH shows hyponatremia with inappropriately concentrated urine 2
• Unlike primary polydipsia, DI patients have inappropriately dilute urine (<200 mOsm/kg) even with dehydration, whereas primary polydipsia patients can concentrate urine when fluid restricted 6