C — Complete absence of the right kidney and right ureter (unilateral renal agenesis).
Without a ureteric bud, there is no WNT9B/FGF2 signal to induce the metanephric blastema, so no nephrons condense. Reciprocal induction fails on that side → no collecting system AND no functional nephrons. The contralateral side compensates (hypertrophy); unilateral disease is usually compatible with life. Bilateral bud failure → bilateral renal agenesis → Potter sequence (oligohydramnios → pulmonary hypoplasia).

C — Pulmonary hypoplasia from oligohydramnios (Potter sequence).
The placenta filters fetal blood during gestation, so the fetus does not die of uremia. After ~20 weeks, amniotic fluid comes almost entirely from fetal urine; without kidneys, oligohydramnios develops → mechanical compression (Potter facies, limb deformities) AND failed amniotic-fluid-driven lung distension → pulmonary hypoplasia = actual cause of neonatal death.

D — The mesonephric (Wolffian) duct is the shared scaffold.
The paramesonephric (Müllerian) ducts descend alongside the mesonephric ducts; partial fusion failure produces a bicornuate uterus. The ureteric bud sprouts from the caudal mesonephric duct; its failure → unilateral renal agenesis. A single Wolffian/paramesonephric disruption can produce both defects on the same side. Always order a renal ultrasound when a Müllerian anomaly is identified.

C — Persistent Müllerian Duct Syndrome (PMDS).
Sertoli cells normally produce MIS (AMH), which triggers regression of the paramesonephric ducts at week 7–8. If MIS is absent (AMH gene mutation) or the MIS type II receptor is nonfunctional, Müllerian structures persist despite otherwise normal male development (testosterone from Leydig → Wolffian SEED; DHT → external male genitalia). Retained Müllerian structures often tether the testes intra-abdominally → cryptorchidism.

A — Complete Androgen Insensitivity (CAIS).
Testes form normally (SRY present). Sertoli cells make MIS → Müllerian regression → no uterus, no upper vagina. Leydig cells produce testosterone normally or high, but the mutant androgen receptor cannot respond → Wolffian ducts regress and external genitalia default to female. Peripheral aromatase converts the high circulating testosterone to estradiol → breast development at puberty. Sparse pubic/axillary hair reflects lost androgen receptor signaling. Inguinal masses = undescended testes.

B — Elevated testosterone-to-DHT ratio (5α-reductase deficiency).
Autosomal recessive loss of 5α-reductase prevents T → DHT conversion in target tissues. Internal Wolffian ducts (T-dependent) form normally; external genitalia (DHT-dependent) do not masculinize until the pubertal T surge directly overwhelms the block. Classic "female at birth, male at puberty"; androgen receptor works (hence muscle/phallus growth, no breast development).

B — Hydrocortisone + fludrocortisone + IV fluids.
This is classic salt-wasting 21-hydroxylase deficiency. Hydrocortisone replaces cortisol AND suppresses ACTH (reducing androgen shunting). Fludrocortisone replaces aldosterone to correct the salt-wasting (hyponatremia, hyperkalemia). Giving testosterone (A) to a virilized 46,XX would worsen virilization. Gonadectomy (C) has no role — gonads are ovaries. Spironolactone (E) would further deplete aldosterone activity.

B — Midline fusion of the metanephric blastemas, caught under the inferior mesenteric artery during ascent.
The patient has Turner syndrome (45,XO): short stature (SHOX haploinsufficiency), streak gonads with hypergonadotropic hypogonadism, webbed neck (cystic hygroma), bicuspid aortic valve + coarctation, and horseshoe kidney. The horseshoe is formed when the lower poles fuse across the midline; the isthmus catches on the IMA → the kidney sits low at L3–L5. Turner patients should have lifelong cardiac monitoring for aortic dissection and renal monitoring for reflux/UTIs.