A 45-year old woman is admitted to the hospital following a head injury. She has severe polyuria (producing 1 L of urine every 2 hours) and polydipsia (drinking 3 to 4 glasses of water every hour).During a 24-hour period in the hospital, the woman produces 10 L of urine, containing no glucose. She is placed on overnight water restriction for fuher evaluation. The following morning, she is weak and confused. Her serum osmolarity is 330mOsm/L, her serum is 164 mEg/L, and her urine osmolarity is 70 mOsm/L. She is treated with dDAVP by nasal spray. Within 24 hours of initiating the treatment, her serum osmolarity is 295mOsm/L and her urine osmolarity is 620mOsm/L.

Following overnight water restriction he striking observation is that the woman is still producing dilute (hyposmotic) urine despite a severely elevated serum osmolarity. Diabetes mellitus is ruled out as cause of her poluria because no glucose is found in her urine. The diagnosis is that the woman has central diabetes insipidus secondary to a head injury. The woman's posterior pituitary gland does not secrete ADH. even with a strong osmotic stimulus such as serum osmolarity of 330mOsm/L. This absence of ADH results in a profound disturbance of water reabsorption, and she is unable to produce concentrated urine. Her distal tubule and collecting ducts are impermeable to water in the absence of ADH, no water can be reabsorbed by these segments, and her urine is hyposmotic (70mOsm/L).Because she is excreting excessive amounts of free water, serum osmolarity and serum increase. The high serum osmolarity is an intense stimulus for thirst, causing the woman to drink water almost continuously.