Wilms Tumour vs Neuroblastoma
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Direct answer
Wilms tumour (nephroblastoma) and neuroblastoma are the two classic abdominal malignancies of early childhood, and NEET-PG loves the contrast. Wilms tumour arises within the kidney, peaks around three to four years, presents as a smooth mass rarely crossing the midline with hypertension and sometimes haematuria, and spreads to lungs; neuroblastoma arises from sympathetic nervous tissue — the adrenal medulla above all — presents earlier, as an irregular mass crossing the midline, secretes catecholamines (urinary VMA and HVA), and spreads to bone, marrow and skull. Both are treated with multimodality therapy and both do well in favourable-risk disease.
What you must remember
- Wilms tumour: renal embryonal tumour peaking at three to four years; painless smooth abdominal mass, hypertension from renin, haematuria, and possible tumour thrombus extending into the renal vein and inferior vena cava.
- Wilms associations: WAGR syndrome (Wilms, aniridia, genitourinary anomalies, intellectual disability), Beckwith-Wiedemann syndrome (hemihypertrophy, macrosomia, omphalocele), Denys-Drash syndrome and isolated aniridia.
- Wilms management: chemotherapy (vincristine with actinomycin D, doxorubicin at higher risk) with nephrectomy and radiotherapy in selected cases; the lung is the dominant metastatic site.
- Neuroblastoma: neural-crest tumour, adrenal medulla commonest; most children are under five years, many under two; an irregular, fixed mass frequently crossing the midline.
- Neuroblastoma markers and spread: urinary vanillylmandelic acid (VMA) and homovanillic acid (HVA) raised; metastases to bone and marrow (pain, limping), skull orbits (periorbital ecchymosis — raccoon eyes) and liver; fine calcification is common on imaging.
- Paraneoplastic syndromes: opsoclonus-myoclonus-ataxia ("dancing eyes, dancing feet") and watery diarrhoea from vasoactive intestinal peptide; hypertension from catecholamines.
- Imaging discriminator: Wilms tumour displaces adjacent vessels, whereas neuroblastoma encases and narrows the aorta and may invade neural foramina (dumbbell tumours).
Common confusion
Age and mass character are the two discriminators candidates fumble: a smooth flank mass in a three-year-old is Wilms, while a hard midline-crossing mass in a one-year-old is neuroblastoma. Hypertension occurs in both — renin in Wilms, catecholamines in neuroblastoma — so the discriminator is the metabolite panel: VMA and HVA are neuroblastoma's fingerprint. Do not forget stage 4S neuroblastoma of infancy — spread to skin, liver and marrow yet capable of spontaneous regression.
Exam-focused takeaway
NEET-PG packages this pair as compare-and-contrast: origin (kidney versus neural crest), age peak (three to four years versus under two), mass character (smooth and unilateral versus irregular and crossing), calcification (uncommon versus common), metastasis (lung versus bone-marrow-skull), markers (none versus VMA/HVA) and the paraneoplastic signs that belong only to neuroblastoma. Vignettes follow the same logic: periorbital bruising with an abdominal mass means neuroblastoma until proven otherwise, while aniridia or hemihypertrophy with a renal mass means Wilms with syndrome workup. Add N-myc amplification as the poor-prognostic one-liner and strong Wilms survival for counselling stems.
Frequently asked questions
Which is the commonest renal tumour of childhood?
Wilms tumour (nephroblastoma), peaking around three to four years and presenting most often as a painless abdominal mass with or without hypertension.
What are raccoon eyes a sign of?
Periorbital ecchymosis from retro-orbital neuroblastoma metastasis — in a child with an abdominal mass it points to neuroblastoma rather than Wilms tumour.
Which urinary metabolites are raised in neuroblastoma?
Vanillylmandelic acid (VMA) and homovanillic acid (HVA), the catecholamine degradation products measured in urine as its biochemical signature.
How do the two masses behave on imaging?
Wilms expands within the kidney and displaces vessels; neuroblastoma encases and narrows the great vessels, invades neural foramina and calcifies more often.
What is stage 4S neuroblastoma?
A special infant pattern with a localised primary plus spread confined to skin, liver and bone marrow — associated with a capacity for spontaneous regression.