Primary Polydipsia (Psychogenic Polydipsia)
Your laboratory values definitively exclude diabetes insipidus and point to primary polydipsia—a behavioral disorder of excessive fluid intake—as the most likely diagnosis. 1
Why Diabetes Insipidus Is Ruled Out
Your test results systematically exclude both central and nephrogenic diabetes insipidus:
Copeptin 4.6 pmol/L is normal and far below the diagnostic threshold. A baseline copeptin >21.4 pmol/L is required to diagnose nephrogenic diabetes insipidus, and your level is less than one-quarter of this cutoff, indicating a normally functioning ADH system. 1, 2
Urine osmolality of 498 mOsm/kg demonstrates intact renal concentrating ability. Diabetes insipidus requires urine osmolality <200 mOsm/kg in the presence of serum hyperosmolality; your kidneys are concentrating urine appropriately, which is pathognomonic against any form of diabetes insipidus. 1, 3
Serum osmolality 301 mOsm/kg with serum sodium 143 mEq/L are both normal. Diabetes insipidus presents with high-normal or elevated serum sodium (>145 mEq/L) and serum osmolality typically >300 mOsm/kg when water access is restricted, but your values indicate normal fluid balance. 1, 4
The combination of normal copeptin, normal serum sodium, and concentrated urine (498 mOsm/kg) is incompatible with any form of diabetes insipidus. 1, 2
Why Primary Polydipsia Fits
Primary polydipsia is characterized by excessive voluntary fluid intake driven by psychological factors, not by physiologic need. Patients drink large volumes despite normal thirst mechanisms and normal ADH secretion. 1, 5
Laboratory findings in primary polydipsia include normal or low-normal serum sodium, normal serum osmolality, and appropriately dilute urine when the patient is overhydrated—but the kidneys retain the ability to concentrate urine when fluid intake is restricted. Your urine osmolality of 498 mOsm/kg after overnight fasting proves this intact concentrating ability. 1, 4
Normal copeptin levels (<21.4 pmol/L) combined with the ability to concentrate urine to >300 mOsm/kg effectively rules out diabetes insipidus and supports primary polydipsia. 2
Recommended Management Algorithm
Step 1: Confirm 24-Hour Urine Output
Document total urine volume with a 3-day frequency-volume chart. Polyuria is defined as >3 L/day in adults; if your output is truly elevated, this confirms the clinical syndrome. 6
Calculate nocturnal polyuria. If >33% of your 24-hour output occurs at night, this suggests a behavioral pattern of excessive nighttime drinking rather than a physiologic disorder. 6
Step 2: Behavioral and Psychiatric Evaluation
Assess for underlying psychiatric conditions. Primary polydipsia is often associated with anxiety disorders, obsessive-compulsive behaviors, or psychotic disorders that drive compulsive water drinking. 5, 7
Review all medications. Certain psychotropic medications (especially antipsychotics) can induce polydipsia as a side effect. 6
Step 3: Fluid Restriction Trial (Under Medical Supervision)
Gradual reduction of fluid intake to normal physiologic levels (approximately 30 mL/kg/day) should resolve polyuria if primary polydipsia is the cause. This must be done under medical supervision to monitor serum sodium and prevent hyponatremia from chronic overhydration. 8
Monitor serum sodium weekly during fluid restriction. Patients with chronic primary polydipsia may have baseline hyponatremia that requires slow correction to avoid osmotic demyelination syndrome. 8
Step 4: Exclude Rare Causes of Polyuria
Measure serum glucose and HbA1c to exclude diabetes mellitus. Your A1c of 5.4% is normal, ruling out osmotic diuresis from hyperglycemia. 9, 6
Check serum potassium, chloride, bicarbonate, and magnesium to exclude Bartter syndrome or other tubulopathies. Your calcium of 9.6 mg/dL is normal, making hypercalcemia-induced polyuria unlikely. 6
Perform renal ultrasound to assess kidney structure and rule out chronic kidney disease. This is particularly important given your normal urodynamics but persistent symptoms. 6
Critical Pitfalls to Avoid
Do not perform a water deprivation test. Your laboratory values already exclude diabetes insipidus, and water deprivation in primary polydipsia can cause dangerous hypernatremia without providing additional diagnostic information. 1, 5
Do not prescribe desmopressin. Desmopressin is ineffective in primary polydipsia and can cause life-threatening hyponatremia by preventing free water excretion in a patient who continues to drink excessively. 1, 6
Do not restrict water access abruptly. Patients with chronic primary polydipsia may have adapted to high fluid intake, and sudden restriction can cause rebound hypernatremia or psychological distress. Gradual reduction under supervision is essential. 8
Long-Term Management
Cognitive-behavioral therapy or psychiatric intervention is the mainstay of treatment for primary polydipsia. Addressing the underlying psychological drivers of excessive drinking is more effective than medical interventions. 5
Regular monitoring of serum sodium and renal function is recommended. Chronic overhydration can lead to hyponatremia and, rarely, to bladder dysfunction from chronic overdistension. 6, 8
Patient education about normal fluid requirements (approximately 2–2.5 L/day for adults) and the risks of excessive water intake is essential. 8