In which type of rickets is calcitriol increased?

In Vitamin D dependent rickets, calcitriol, which is the active form of Vitamin D, is usually elevated. This condition arises from a genetic defect in the ability of the body to use Vitamin D effectively, leading to impaired calcium absorption and subsequent bone mineralization. The body compensates for low calcium levels by increasing the production of calcitriol in an attempt to enhance calcium absorption in the intestines, despite the underlying defect that hinders its use.

In contrast, Vitamin D independent rickets is characterized by an inability to respond to Vitamin D effectively, so calcitriol would not be elevated; instead, it would remain low due to the presence of a different mechanism affecting bone mineralization. Hypophosphatemic rickets, on the other hand, is generally accompanied by normal or low levels of calcitriol because the primary defect lies in phosphate reabsorption rather than a defect in Vitamin D metabolism. Osteomalacia, which occurs in adults, involves a deficiency of Vitamin D or calcium, often resulting in low calcitriol rather than elevated levels.

Thus, in Vitamin D dependent rickets, the elevation of calcitriol represents the body's adaptive response to combat the effects of the Vitamin D metabolic defect and to try and normalize