In Classic Salt Wasting Congenital Adrenal Hyperplasia, which hormone is primarily deficient, leading to salt loss through urine?

In Classic Salt Wasting Congenital Adrenal Hyperplasia (CAH), the primary hormone that is deficient is aldosterone. This condition arises due to a genetic enzyme deficiency, most commonly 21-hydroxylase, which leads to impaired adrenal synthesis of cortisol and aldosterone.

The deficiency of aldosterone specifically results in the kidneys being unable to properly retain sodium. As aldosterone plays a crucial role in sodium reabsorption, its deficiency primarily manifests as a loss of sodium, which is excreted in the urine. This can lead to hypovolemia, hypotension, and an increase in renin levels as the body attempts to compensate for the low sodium levels.

Even though cortisol and androgens are also affected due to the enzymatic block, it is the lack of aldosterone that directly results in salt wasting, making it the most pertinent hormone deficiency to this specific symptom of the classic form of CAH.