Diabetes insipidus (DI) presents as polyuria, the passing of abnormally large volumes of urine, together with polydipsia, the drinking that follows the loss of water. The urine is dilute, or hypotonic, and this combination of a large volume with a low urine osmolality (the concentration of dissolved particles in the urine) is what separates DI from the other causes of passing a lot of urine.
The volume of urine
The urine flow rate in DI is in the range of 40 ml/kg per 24 hours in adults and 100 ml/kg per 24 hours in infants. The polyuria is continuous rather than episodic and, in central and nephrogenic DI, it continues at night as nocturia, waking from sleep to pass urine.
Why the plasma sodium usually stays normal
In central and nephrogenic DI the thirst mechanism is intact, so patients drink enough to replace the water they lose and the plasma osmolality and sodium remain normal; polyuria and thirst are then the main complaints. Hypernatremia, a raised plasma sodium concentration, develops only when the lost water cannot be replaced: when thirst is impaired, for example in an unconscious or confused patient, or when water is simply not available. Patients with nephrogenic DI, especially those taking lithium, are more vulnerable to it than patients with central DI.
Dipsogenic disease
Dipsogenic DI produces the same hypotonic polyuria through a different route: an exaggerated thirst drives a fluid intake large enough to suppress ADH. The polyuria is confined to the daytime and follows the drinking, rather than continuing through the night.
The three forms therefore look alike at the bedside and differ in where the failure lies: in ADH secretion, in the kidney’s response to ADH, or in the amount drunk.