Urinary kallikrein excretion after DDAVP during lithium treatment

Several factors are believed to contribute to impaired responsiveness to arginine vasopressin (AVP) during lithium treatment. The renal kallikrein–kinin system is reported to antagonize the renal effects of AVP in vitro but there are no reports of its activity during lithium treatment. Urinary active kallikrein excretion in 18 lithium-treated patients was found to be lower than that in eight healthy volunteers. Following intravenous administration of an AVP analogue, des-amino-D-arginine-vasopressin, to the lithium-treated patients, the urinary excretion of active kallikrein was unchanged, despite an impaired urine-concentrating ability. These results suggest that stimulation of renal kallikrein does not contribute to inhibition of the action of AVP, and thus the genesis of nephrogenic diabetes insipidus during lithium treatment.