**Core Concept**
Virilization and hypertension with low plasma renin are hallmark features of 11β-hydroxylase deficiency, a congenital adrenal hyperplasia (CAH) disorder due to impaired cortisol synthesis, leading to accumulation of 11-deoxycortisol and excess androgen production.

**Why the Correct Answer is Right**
In 11β-hydroxylase deficiency, the enzyme that converts 11-deoxycortisol to cortisol is deficient. This results in shunting of precursors toward androgen synthesis, causing virilization in females. The lack of cortisol suppresses renin release, leading to low plasma renin and secondary hypertension. The elevated androgens cause masculinization, while the low renin and high aldosterone (due to compensatory mechanisms) cause hypertension.

**Why Each Wrong Option is Incorrect**
Option A: 21α-hydroxylase deficiency causes salt-wasting and virilization but typically presents with hyponatremia, hyperkalemia, and low renin — not the classic low renin hypertension pattern.
Option C: 3β-hydroxylase deficiency results in 17α-hydroxyprogesterone accumulation and virilization, but hypertension is not a key feature; renin levels are usually normal or elevated.
Option D: Conn’s syndrome (primary hyperaldosteronism) presents with hypertension, low potassium, and **high** plasma renin — opposite to the given low renin profile.

**Clinical Pearl / High-Yield Fact**
In CAH, virilization with low renin and hypertension points to 11β-hydroxylase deficiency. Remember: low renin + virilization = 11β-hydroxylase deficiency; high renin + hypertension = Conn’s syndrome.

✓ Correct Answer: B. 11 β hydroxylase deficiency