This is a rare condition caused by deficiency of ADH; over 90% of the neurons synthesizing vasopressin must be destroyed in order to produce ADH deficiency and cause polyuric symptoms (1). ADH can be detected in the plasma but at concentrations which are low for the plasma osmolality. Urine output ranges from 3-15 litres per 24 hours causing hypertonic dehydration and secondary polydipsia.
Adequate fluid intake permits most patients to achieve normonatraemia. Occasionally, hypothalamic disease may damage the thirst centre and/or the osmoreceptors resulting in hypernatraemia; this may also develop in patients denied access to water.
Be aware that the condition may be masked in patients with concomitant adrenocortical insufficiency as this impairs the ability of the kidney to excrete water. Features of CDI become apparent when corticosteroid replacement therapy is instigated.
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