They demonstrated that the patients with impaired ADH suppression who failed to develop hyponatremia exhibited higher dietary sodium intake and lower natriuresis compared with hyponatremic patients, suggesting that the pathophysiology of post-transsphenoidal hyponatremia is complex and multifactorial and not due only to impaired ADH suppression, but instead displaying features of both SIADH and CSW [21]. Here, AVP is linked to Hyponatremia.