What does a patient with diabetes insipidus complain of?
A healthy kidney takes back most of the water it filters, and ADH lets the collecting duct return the last part, leaving a small volume of concentrated urine. In diabetes insipidus (DI) that last step fails, or ADH is switched off. The kidney then loses water, and thirst follows the loss. So DI presents as polyuria together with polydipsia: passing abnormally large volumes of urine, and drinking that follows the loss of water.
The urine is dilute, that is, hypotonic. A large urine volume with a low urine osmolality is what separates DI from other causes of passing a lot of urine. To give a sense of scale, 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.
Why does the polyuria carry on at night?
The dilute urine does not stop when the patient goes to sleep. The polyuria of DI is continuous rather than episodic, because the kidney’s failure to concentrate urine does not depend on the time of day. In central and nephrogenic DI the polyuria therefore continues at night as nocturia, waking from sleep to pass urine.
Why does the blood sodium usually stay normal?
If urine is lost all the time, what keeps the patient from drying out? Thirst. In central and nephrogenic DI the thirst mechanism is intact. Because thirst is intact, patients drink enough to replace the lost water, so plasma osmolality and sodium remain normal. Polyuria and thirst are then the main complaints.
When does hypernatremia appear?
Thirst is the safety valve, so what happens when it fails or when water is missing? The urine loss goes on, but the intake no longer matches it. Hypernatremia develops only when lost water cannot be replaced. That happens in two situations: when thirst is impaired, for example in an unconscious or confused patient, and when water is simply not available. Both are the same problem, a continuing loss without replacement.
Patients with nephrogenic DI, especially those taking lithium, are more vulnerable to hypernatremia than patients with central DI. No explanation for this difference is given here.
How does dipsogenic DI look different?
So far thirst follows the loss. What if it leads? Dipsogenic DI produces the same hypotonic polyuria through a different route. Exaggerated thirst drives a fluid intake large enough to suppress ADH, and with ADH suppressed the kidney makes dilute urine. The urine therefore follows the drinking. Polyuria in dipsogenic DI is confined to the daytime, when the patient drinks, rather than continuing through the night as it does in central and nephrogenic DI.
Why do the forms look the same?
The daytime-only pattern is a clue, but at the bedside the three forms look alike. They differ in where the failure lies: ADH secretion, the kidney’s response to ADH, or the amount drunk. These are three different steps in one loop, so the same symptoms can come from different failures. When the failure is ADH secretion itself, what damages the cells that make the hormone, and what happens to the urine after pituitary surgery?