Do I have undiagnosed diabetes insipidus given my normal serum sodium, urine osmolality, and copeptin levels after a 12-hour fast, with a history of anxiety and potential psychogenic polydipsia?

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You Do Not Have Diabetes Insipidus

Your laboratory results definitively exclude diabetes insipidus—your urine osmolality of 498 mOsm/kg demonstrates excellent kidney concentrating ability, which is incompatible with any form of diabetes insipidus. 1

Why Your Results Rule Out Diabetes Insipidus

  • Urine osmolality >300 mOsm/kg rules out diabetes insipidus, and your value of 498 mOsm/kg indicates completely normal kidney concentrating ability after your 12-hour fast 1

  • The pathognomonic triad of diabetes insipidus requires: polyuria (>3 liters/24 hours), inappropriately dilute urine (osmolality <200 mOsm/kg), and high-normal or elevated serum sodium—none of which you meet 2, 1

  • Your copeptin level of 4.6 pmol/L is normal and falls well below the 21.4 pmol/L threshold that would suggest nephrogenic diabetes insipidus 2, 1

  • Your serum sodium of 143 mEq/L and serum osmolality of 301 mOsm/kg are both normal, and when combined with appropriately concentrated urine, this combination is completely inconsistent with diabetes insipidus 1

Understanding Your Test Results

  • In true diabetes insipidus, urine osmolality remains <200 mOsm/kg even with dehydration or fasting, because the kidneys cannot concentrate urine due to either ADH deficiency (central DI) or ADH resistance (nephrogenic DI) 2, 3

  • Your kidneys responded appropriately to the 12-hour fast by concentrating your urine to 498 mOsm/kg, proving that both your ADH secretion and kidney response to ADH are functioning normally 1

  • Proceeding with a formal water deprivation test would be uncomfortable and potentially dangerous without adding any diagnostic value when baseline testing already shows urine osmolality >300 mOsm/kg with normal serum osmolality 1

What Your Results Actually Suggest

  • Given your history of anxiety and the normal laboratory findings, primary polydipsia (psychogenic polydipsia) is the most likely explanation for any excessive thirst or urination you may be experiencing 2, 4

  • Primary polydipsia is characterized by excessive fluid intake driven by psychological factors or abnormal thirst regulation, not by a defect in ADH secretion or kidney function 3, 4

  • In primary polydipsia, patients can concentrate their urine normally when fluid intake is restricted, which is exactly what your results demonstrate 4

Critical Pitfall to Avoid

  • Do not confuse diabetes insipidus with diabetes mellitus—diabetes mellitus causes polyuria through osmotic diuresis from glucose spilling into urine (requiring fasting glucose ≥126 mg/dL), whereas diabetes insipidus causes polyuria from inability to concentrate urine due to ADH problems 2, 1

Recommended Next Steps

  • Measure your actual 24-hour urine volume to objectively quantify whether you truly have polyuria (>3 liters/24 hours in adults), as perceived excessive urination may not meet clinical thresholds 2, 1

  • Investigate alternative causes of your symptoms such as medications, caffeine intake, or behavioral patterns related to your anxiety that may be driving excessive fluid intake 1

  • If you have genuine concerns about excessive thirst despite these normal results, consider evaluation for other conditions that can affect fluid balance, such as hypercalcemia (your calcium of 9.8 mg/dL is normal), hypokalemia, or early chronic kidney disease—though your results make these unlikely 1

References

Guideline

Diagnosis and Exclusion of Diabetes Insipidus

Praxis Medical Insights: Practical Summaries of Clinical Guidelines, 2026

Guideline

Management of Diabetes Insipidus

Praxis Medical Insights: Practical Summaries of Clinical Guidelines, 2025

Research

Diabetes insipidus.

Annales d'endocrinologie, 2013

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This information is intended for healthcare professionals. Any medical decision-making should rely on clinical judgment and independently verified information. The content provided herein does not replace professional discretion and should be considered supplementary to established clinical guidelines. Healthcare providers should verify all information against primary literature and current practice standards before application in patient care. Dr.Oracle assumes no liability for clinical decisions based on this content.

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