Diabetes insipidus (DI) is a syndrome characterised by polyuria, excessive thirst and polydipsia.
Central or neurogenic DI results from inappropriately low ADH release into the circulation.
Nephrogenic DI results from deficient action of ADH
Actions of ADH
Antidiuresis
ADH acts on V2 receptors in the distal renal tubule, mainly in the collecting duct.
V2 agonist action increases transcription and insertion of water channels (Aquaporin-2) into the apical membrane of collecting tubule and collecting duct epithelial cells.
Aquaporins allow water to move down their osmotic gradient and out of the nephron, increasing the amount of water re-absorbed from the filtrate back into the bloodstream
Vasoconstriction
Vasoconstriction results from V1a receptor stimulation. This becomes relevant in hypotensive states where high concentrations of ADH contribute to the maintenance of blood pressure.
Coagulation
Coagulation effects are extrarenal V2 receptor-mediated. Prostacyclin generation is stimulated. TPA, Factor VIII and VWF multimers all increase. Desmopressin is the treatment of choice for patients with type I and type II von Willebrand’s disease