A 28-year-old man with a history of type 1 diabetes presents with polydipsia and polyuria for the last 5 weeks. The patient reports that his blood glucose levels have been well controlled on his current insulin regimen. The patient denies tobacco, alcohol, or drug use and has no other past medical history. He has a temperature of 36.8°C, blood pressure of 114/68 mmHg, heart rate of 96 beats per minute, respiratory rate of 16 breaths per minute, and oxygen saturation of 98% on room air. The patient reports that he has fasted for the visit and laboratory results reveal the following:
Desmopressin was administered and 30 minutes later the urine osmolality is 432 mOsm/kg.
Which of the following is this patient’s diagnosis?
A. Primary polydipsiaCentral diabetes insipidus. The patient in this question presents with polyuria and polydipsia with a normal serum glucose level. Given the patient’s hypernatremia, low urine osmolality, and elevated serum osmolality, the patient likely has diabetes insipidus (DI) and it now remains to distinguish between central and nephrogenic DI.
(A) Primary polydipsia is not the answer here because in primary polydipsia you would expect hyponatremia given that the increased water consumption in primary polydipsia overwhelms the capability of the kidneys to excrete the water. (D) SIADH is incorrect for the same reason—you would expect hyponatremia and this patient has hypernatremia (sodium >145 mEq/L). Central DI occurs when the pituitary gland does not secrete sufficient ADH. Nephrogenic DI occurs when the nephrons themselves show resistance to ADH (but ADH levels will be normal because the pituitary gland is functionally intact). In nailing the diagnosis, the patient must first engage in a water deprivation test for at least 2 hours. If the urine osmolality is >600 mOsm/kg at the conclusion of the test, then the diagnosis is likely primary polydipsia since the patient is able to concentrate urine without water intake. If the urine is still dilute (<600 mOsm/kg) at the end of the water deprivation test, then desmopressin (synthetic vasopressin) is administered and urine osmolality is monitored. If urine osmolality increases, then this proves that pituitary secretion of ADH is deficient and central DI is diagnosed. Nephrogenic DI will have negligible change in urine osmolality since the problem is renal pathology (not the amount of ADH). The patient in this question has a urine osmolality that increased about 400% after desmopressin, establishing the diagnosis as central DI.