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Dysfunction is caused when the tumor compresses the normal kidney parenchyma.The mesenchymal component may include cells showing rhabdomyoid differentiation or malignancy (rhabdomyosarcomatous Wilms).Wilms tumors may be separated into two prognostic groups based on pathologic characteristics:
Favorable – Contains well developed components mentioned above
Anaplastic – Contains diffuse anaplasia (poorly developed cells)

Molecular biology and related conditions
Mutations of the WT1 gene which is located on the short arm of chromosome 11 (11p13) are observed in approximately 20% of Wilms tumors, the majority of them being inherited from the germline, while a minority are acquired somatic mutations. In addition at least half of the Wilms tumors with mutations in WT1 also carry acquired somatic mutations in CTNNB1, the gene encoding the proto-oncogene beta-catenin. This latter gene is found on short arm of chromosome 3 (3p22.1). Most cases do not have mutations in any of these genes. An association with H19 has been reported. H19 is a long noncoding RNA located on the short arm of chromosome 11 (11p15.5). Diagnosis
The majority of people with Wilms tumor present with an asymptomatic abdominal mass which is noticed by a family member or healthcare professional. Renal tumors can also be found during routine screening in children who have known predisposing clinical syndromes. The diagnostic process includes taking a medical history, a physical exam, and a series of tests including blood, urine, and imaging tests.Once Wilms tumor is suspected, an ultrasound scan is usually done first to confirm the presence of an intrarenal mass.