Path Renal 3

Front 1

Small, discrete cortical tumors
Arise from the renal tubular epithelium
Most frequently papillary

Back 1

Renal adenoma

Front 2

Renal adenoma morphology

Back 2

Complex, branching, papillomatous structures with numerous complex fronds

Front 3

Present in 25% to 50% of patients with tuberous sclerosis, a disease characterized by
Lesions of the cerebral cortex
Skin abnormalities

Back 3

Angiomyolipoma
Benign tumor consisting of
Vessels
Smooth muscle
Fat

Front 4

Epithelial tumor Tan or mahogany brown with a central scar

Back 4

Oncocytoma. Arise from the intercalated cells of collecting ducts

Front 5

Oncocytoma are composed of

Back 5

-Composed of large, eosinophilic cells having small, round, benign-appearing nuclei that have large nucleoli
-, the eosinophilic cells have numerous mitochondria
-Familial cases may be multicentric

Front 6

Generally 0.5 cm in size or less
Spindle cells in loose stroma with entrapped tubules

Back 6

Medullary Fibroma. Incidental finding also called a renomedullary interstitial cell tumor
Not associated with any renal diseases

Front 7

Hematuria with palpable mass, flank pain, long standing fever and associated with paraneoplastic syndromes

Back 7

Renal cell carcinoma (adenocarcinoma of the kidney) which arises from tubular epithelium
Associated with von Hippel Lindau disease.
Most common in men in their 60s and it is the most common renal malignancy

Front 8

Main risk factors for renal cell carcinoma

Back 8

Tobacco is the most significant risk factor (double)
Obesity (particularly in women)
Hypertension
Unopposed estrogen therapy
Exposure to asbestos, petroleum products, and heavy metals
Increased incidence in patients with chronic renal failure

Front 9

Von Hippel-Lindau (VHL) syndrome

Back 9

hemangioblastomas of the cerebellum and retina
renal cysts
bilateral, often multiple, renal cell carcinomas (nearly all, if they live long enough)
current studies implicate the VHL gene in the development of both familial and sporadic clear cell tumors.

Front 10

Renal Cell Carcinoma most cases are due to

Back 10

sporadic reasons. 98% of these tumors, whether familial, sporadic, or associated with VHL, there is loss of sequences on the short arm of chromosome 3
VHL gene acts as a tumor-suppressor gene

Front 11

Papillary carcinoma sporadic form genetic bases

Back 11

Trisomies 7, 16, and 17 and loss of Y in male patients

Front 12

Papillary carcinoma familial genetic bases

Back 12

The gene for the familial form has been mapped to a locus on chromosome 7, encompassing the locus for MET
a protooncogene
tyrosine kinase receptor for hepatocyte growth factor.
mutated in a proportion of the sporadic cases
hepatocyte growth factor (also called scatter factor) mediates growth, cell mobility, invasion

Front 13

grow from intercalated cells of collecting ducts
excellent prognosis
histologic distinction from oncocytoma can be difficult.

Back 13

Chromophobe renal carcinoma

Front 14

Carcinoma of collecting duct cells in the medulla
medullary location.

Back 14

Collecting duct (Bellini duct) carcinoma

Front 15

Where does renal cell carcinoma spread to?

Back 15

Lungs (more than 50%)
Bones (33%)
Rregional lymph nodes
Liver
Adrenals
Brain

Front 16

Huge palpable flank mass in a young child and microscopic hematuria

Back 16

Wilms tumor. Most common primary renal tumor of childhood
4th most common pediatric malignancy in US
2-5 years

Front 17

Wilms tumor is caused by

Back 17

deletion of WT-1 gene (tumor suppressor) on short arm of chr 11.

Front 18

Denys-Drash syndrome

Back 18

90% risk of Wilms tumor
Gonadal dysgenesis
Early onset nephropathy (Diffuse mesangial sclerosis)
Germline abnormality of WT1
Increased risk of gonadoblastomas

Front 19

Organomegaly
Macroglossia
Hemihypertrophy
Omphalocele
Chromosome 11 band p15.5 (WT2)
Abnormality of genomic imprinting

Back 19

Beckwith-Weidemann syndrome

Front 20

papillomas to invasive carcinomas
noticeable hematuria

Back 20

Urothelial Carcinomas of the Renal Pelvis

Front 21

Painless hematuria; irritative voiding symptoms, palpable mass, hepatomegaly

Back 21

Transitional cell carcinoma. Associated with smoking, exposure to aniline dyes, cyclophosphamide and phenacetin abuse.

Front 22

Scattered small cortical and medullary cysts with hyperplastic or flattened epithelium
0.5 to 2 cm in size
Cysts contain clear fluid and calcium oxalate crystals

Back 22

Acquired (dialysis-associated) cystic disease

Front 23

Acquired (dialysis-associated) cystic disease forms due to

Back 23

obstruction of tubules by interstitial fibrosis or by crystals

Front 24

Autosomal dominant disease with APKD1 gene mutation on chromosome 16

Back 24

Autosomal-dominant (adult) polycystic kidney disease (ADPKD)
Infantile form is autosomal reccesive PKHD1 maps to
chromosome 6p21-23
novel protein, fibrocystin

Front 25

Whats the pathology of Autosomal-dominant (adult) polycystic kidney disease (ADPKD)?

Back 25

Replacement of renal parenchyma bilaterally with multiple large variably size cysts

Front 26

Infantile polycystic kidney disease (ADPKD) pathology

Back 26

closed, small, homogenous cysts that are not in continuity with the collecting system

Front 27

CT with multiple cysts at birth

Back 27

Infantile polycystic kidney disease (ADPKD). Results in death shortly after birth

Front 28

Hypertension, hematuria, and palpable renal mass. CT scan shows multiple cysts in both kidneys

Back 28

Autosomal-dominant (adult) polycystic kidney disease (ADPKD)?

Front 29

Autosomal-dominant (adult) polycystic kidney disease (ADPKD) is associated with

Back 29

secondary polycythemia, polycystic liver disease, berry aneurysms and mitral valve prolapse.