Central diabetes insipidus (CDI) is a rare disease characterised by the excretion of copious amounts of diluted urine (polyuria), excess water intake (polydipsia), and a rise in serum sodium concentration (hypernatremia) (Christ-Crain et al., 2019). The neuropeptide arginine-vasopressin (AVP) is synthesised as a preprohormone along with its carrier protein neurophysin II (NPII) in hypothalamic supraoptic (SON) and paraventricular (PVN) magnocellular neurons, stored in the posterior pituitary, and secreted into the circulation. It binds to AVP receptor 2 in the kidney to promote the insertion of aquaporin channels (AQP2) that mediate antidiuretic effects. AVP production and secretion deficits cause CDI, while renal insensitivity to the antidiuretic effect of AVP causes nephrogenic diabetes insipidus (NDI) (Mahia and Bernal, 2021). Mice and rats carrying spontaneous or engineered mutations in the AVP-NPII gene present phenotypes similar to those of CDI patients (Valtin and Schroeder, 1964; Russell et al., 2003). However, the pathogenesis and complex clinical manifestations of CDI remain poorly understood.