Neoplasms of the kidney
Benigns
Renal papillary adenoma
• Small, discrete adenomas
• Renal tubular epithelium
• Papillary pattern
• Most patients >70 yo
Pathogenesis:
Loss of chromosome Y
Gains of chromosomes 7 and 17
Morphology:
• Small tumors (<0.5 cm).
• Within the cortex.
• Pale yellow-gray, discrete, well-
circumscribed nodules.
• Complex, branching, papillomatous
structures.
• Cells grow as tubules, glands, cords, and
sheets.
• Cuboidal to polygonal cell shape.
• Regular, small central nuclei
• Scanty cytoplasm, and no atypia.
Angiomyolipoma Oncocytoma
• Vessels, smooth muscle, and adipose tissue • Epithelial neoplasm.
• Tuberous sclerosis • Large eosinophilic cells.
• Small, round, benign-appearing nuclei, large
Morphology: nucleoli.
• Focal areas of mature adipose tissue.
• Smooth muscle cells appear radiate from Morphology:
vessel walls. • Tan or mahogany brown.
• Thickened and hyalinized vessels with • Homogeneous and well encapsulated.
eccentric lumens. • Central scar.
• Mitotic activity is rare. • Large size (up to 12 cm).
Clinical course: Pathogenesis:
• Spontaneous hemorrhage • Alterations of chromosomes 1, Y, and 14.
• Retroperitoneal hemorrhage • Chromosomal translocations t (5;11) and t (9;11).
• Renal failure • Solid nests, tubules, and acini of variable size.
• Hypocellular hyalinized or myxoid stroma.
• Numerous mitochondria.

Renal cell carcinomas
• Older individuals
• 2:1 male preponderance
Epidemiology:
• Tobacco is the most significant risk factor
• Most sporadic
• Usual forms of autosomal dominant familial
cancers
 Von hipple-lindau (VHL) syndrome
 Hereditary leiomyomata and renal cell
cancer syndrome
 Hereditary papillary carcinoma
 Birth-hogg dubé syndrome
Malignant
Clear Cell Renal Carcinoma Papillary carcinoma
• Most common type. • Papillary growth pattern.
• Clear or granular cytoplasm and nonpapillary pattern. • Familial and sporadic forms.
• Most cases are sporadic. • Multifocal in origin.
• Loss of sequences on chromosome 3. • Sporadic: Trisomies 7 and 17, and loss of Y.
• VHL gene deletions. • Familial: Trisomy 7 (MET gene)
Morphology: Morphology:
• Well-circumscribed tumors. • Tumor >4 cm well circumscribed.
• Characteristic golden yellow color is readily identified. • Brown hemorrhagic cut surface.
• Areas of hemorrhage and necrosis. • Hemorrhage and cystic degeneration
• Cystic change areas are also apparent. • Frank necrosis.
• Calcification and even ossification. • Tubular and papillary architecture.
• Cortical protrusion. • Multiple tubules and/or papillae.
• Mean size 7 cm • Cholesterol clefts and foamy histiocytes.
• Nested / alveolar patterns to solid growth patterns. • Hemosiderin granules and calcified concretions
• Delicate vascular network. (psammoma bodies).
• Cells with high lipid and glycogen content.
• Accentuate the cell border Clinical features:
• Upper pole preponderance
Clinical features: • Clinical manifestations similar to CCC
Hematuria.
Silent until it attains a large size.
Nonspecific findings, such as fatigue, weight loss; fever, and
anorexia.
Paraneoplastic syndromes.
Tendency to metastasize widely

Chromophobe carcinoma
• Sixth decade of life.
• Multiple chromosome losses and extreme
hypodiploidy.
• Excellent prognosis compared with CCC and PC.
• Prominent cell membranes.
• Pale eosinophilic cytoplasm.
• Halo around the nucleus.
Morphology:
 Solitary, well-circumscribed, solid appearing.
 Light-tan to tan-brown in color.
 Soft consistency ("spongy").
 Mean size of 7 to 8 cm.
 Diffuse, solid sheet-like appearance.
 Interspersed medium-sized blood vessels.
 abundant flocculent cytoplasm.
 Cell membrane accentuation ("vegetable
cells").
 Irregular nuclear outline, coarse chromatin
pattern ("koilocytic").
 Prominent nucleoli.
 Binucleation is common, but mitotic activity is
rare.
Pathogenesis:
 Loss of whole chromosomes
 Losses of chromosomes 1,2,6,13,17, and 21
Clinical features:
 Clinical presentation like other RCCs
 Mean age 59 yrs
Malignant
Xp11 Translocation Carcinoma Collecting Duct Carcinoma
• Young patients. • Prognosis is dismal.
• Translocations of the TFE3 gene located at Xp11.2 • Malignant cells forming glands enmeshed.
• Overexpression of the TFE3 transcription factor. • Prominent fibrotic stroma, in a medullary
• Clear cytoplasm, papillary architecture. location.
• Prominent psammoma bodies.
Morphology:
 Size from 2 to 12 cm.
 Midportion location.
 Extensive involvement of the medulla.
 Invasion into the renal pelvis.
 Firm gray to tan-white appearance.
 Infiltrative borders.
 Satellite nodules.
 Areas of necrosis
 Diagnosis of exclusion.
 Angulated tubular and glandular structures
 Desmoplastic stroma and fibrosis.
 Neutrophilic inflammatory infiltrate.
 Nuclei with clear chromatin.
 Prominent nucleoli.
 Apoptosis and mitotic activity are readily
identified.
Clinical features:
Aggressive renal carcinoma
Clinical evidence of metastases
Midportion predilection
Flank mass, abdominal pain, weight loss.
Hematuria.
 Malignant
Urothelial Carcinoma
• From benign papilloma to invasive urothelial carcinomas.
• Clinically apparent within a short time.
• Noticeable hematuria.
• Small when discovered.
• May block the urinary outflow.
• Hydronephrosis and flank pain.

Clinical features:
 Increased incidence Lynch syndrome and analgesic nephropatity.
 Infiltration of the wall of the pelvis and calyces.
 The prognosis is not good.