In central/neurogenic DI, what is the primary issue regarding ADH?

In central or neurogenic diabetes insipidus (DI), the primary issue involves the lack of production of antidiuretic hormone (ADH) by the posterior pituitary gland. In this condition, damage to the hypothalamus or pituitary gland leads to a deficiency in the secretion of ADH, which is crucial for regulating water balance in the body. Without adequate amounts of ADH, the kidneys are unable to concentrate urine, resulting in excessive water loss and subsequently, symptoms of polyuria and polydipsia.

Understanding the role of ADH is key in this context. ADH normally facilitates the reabsorption of water in the kidneys' collecting ducts, thereby reducing urine output and maintaining fluid balance. When ADH is deficient, the kidneys fail to perform this function, leading to increased urine production and, consequently, dehydration and thirst as the body attempts to compensate for fluid loss.

In contrast, conditions related to excessive production or resistance to ADH pertain to other forms of diabetes insipidus or different pathophysiological mechanisms entirely. Therefore, the identification of the lack of production of ADH in central/neurogenic DI highlights the underlying issue contributing to the disorder.