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Pathology > Renal > Flashcards

Renal Flashcards

1
Q

Diminished renal reserve (GFR, BUN, Creatinine, presentation)

A

GFR is 50%, BUN and creatinine are normal, asymptomatic

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2
Q

Renal insufficiency (GFR, BUN, creatinine, presentation)

A

GFR is 20-50% of normal. Anemia and HTN. Polyuria and nocturia

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3
Q

Chronic renal failure (GFR, BUN, creatinine, presentation)

A

GFR is <20-25% of normal. Edema, acidosis, hyperkalemia, uremia with neuro, GI and CV complications

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4
Q

End stage renal disease (GFR, BUN, creatinine, presentation)

A

GFR < 5%, terminal stage of uremia

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5
Q

Nephritic syndrome

A

hematuria, azotemia, variable proteinuria, oliguria, edema, HTN –> glomerular

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6
Q

Nephrotic syndrome

A

> 3.5 g/day proteinuria, hypoalbuminemia, hyperlipidemia, lipiduria

  • comes from increased permeability to plasma proteins with massive proteinuria
  • sodium and water retention
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7
Q

Poststreptococcal Postinfectious Glomerulonephritis (acute proliferative)

A

Onset: 1-4 weeks post strep infection
Age: 6-10 years of age
Types: 12, 4, 1 of M protein of cell wall
Path: immune mediated nephritic syndrome
Light microscopy: enlarged hypercellular glomeruli with infiltration of leukocytes (neutrophils and monocytes), proliferation of endo and mesangial cells, severely crescent formation
IF: granular IgG and C3 in mesangium
EM: electron dense deposites in subepi humps
Course: 1. malaise, fever, nausea, oliguria, hematuria with red cell casts in urine, proteinuria, periorbital edema, mild HTN –> children
2. HTN or edema with increased BUN –> adults
Prognosis: full recovery in 95% or get rapidly progressive glomerulonephritis –>children
full recovery in 60% or go to proteinuria, hematuria, HTN–> adults

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8
Q

Nonstreptococcal acute glomerulonephritis

A

similar to poststrep –> staph endocarditis, pneumo, meningococcemia, hep B, hep C, mumps, HIV, varicella, IM, malaria, toxoplasmosis
IF: subepi humps

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9
Q

Rapidly progressive glomerulonephritis

A

Age: any age
Onset: rapid
Path: immune mediated, severe glomerular injury
3 types: Type I –> anti GBM antibody (goodpastures)
Type II –> immune complex (post infectious GN, lupus, henoch schonlein purpura
Type III –> pauci immune (ANCA, wegeners, microscopic polyangiitis)
Light Microscopy: crescent formation with fibrin strands between cellular layers, ruptures in GBM
Clinical: hematuria with red blood cell casts, moderate proteinuria, variable HTN and edema

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10
Q

Goodpasture’s syndrome

A

Clinical presentation: Anti GBM antibody, Type I RPGN
Path: alpha3 chain of collagen type IV
Light microscopy: extracapillary proliferation with crescents and necrosis
IF: linear IgG and C3, fibrin in crescents
EM: no deposits, GBM disruptions, fibrin
Clinical: recurrent hemoptysis or pulmonary hemorrhage

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11
Q

Type II RPGN

A

immune complex deposition: IgA, henoch schonlein, postinfectious, lupus
IF: granular staining
Light microscopy: crescent formation

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12
Q

Type III RPGN

A

Clinical presentation: pauci immune, nothing there, have ANCAs
Diseases: Wegeners granulomatosis, microscopic polyangiitis

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13
Q

Membranous nephropathy

A

Age: adults mostly
Clinical: nephrotic syndrome, characterized by diffuse thickening of glomerular capillary wall
Path: immune complex formation of Ig deposits along subepi side of BM
Associated with: drugs (penicillamine, captopril, gold, NSAIDS), underlying malignant tumors (colon, lung, melanoma CA), SLE, infections (Hep B, HepC, syphilis, schistosomosiasis, malaria), other autoimmune
Light microscopy: diffuse capillary thickening
IF: granular IgG and C3, diffuse
EM: subepi deposits
Clinical: hematurai, mild HTN, not responding to corticosteroids

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14
Q

Minimal change disease

A

Age: children mostly, 2-6
Clinical: most frequent cause of nephrotic syndrome in children –> responds to corticosteroid therapy
Path: effacement of foot podocytes/ processes of epi visceral cells –> probably immune to nephrin or podocin
Associated with: respiratory infections, eczema/rhinitis, HLA haplotypes, Hodgkin lymphoma with T cell mediated immunity,
Light microscopy: normal
IF: negative
EM: loss of foot processes
Course: proteinuria may recur

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15
Q

Focal segmental glomerulosclerosis

A

Clinical: most common adult nephrotic syndrome, lesion characterized by sclerosis of some glomeruli and portion of glomeruli
Path: visceral epithelial cell damage
Types: idiopathic; associated with HIV, heroin, sickle cell, massive obesity; scarring of necrotizing lesions (IgA nephropathy); reflux nephropathy, hypertensive nephropathy, unilateral renal agenesis; inherited from podocin NPHS2, actinin, nephrin NPHS1
- collapsing glomerulopathy characterized by retration and/or collapse of glomerular tuft
IF: focal; IgM and C3
EM: loss of foot processes, epi denudation
Light microscopy: focal and segmental sclerosis and hyalinosis, collapse of capillary loops
Course: higher hematuria, reduced GFR, hypertension, proteinuria nonselective, poor response to corticosteroid, progression to chronic kidney disease

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16
Q

HIV associated nephropathy

A

acute renal failure, acute interstitial nephritis, thrombotic microangiopathies, postinfectious glomerulonephritis and most commonly severe form of collapsing FSGS

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17
Q

Membranoproliferative glomerulonephritis (Type I)

A

Age: young adults
Clinical: Nephrotic/ nephrotic syndrome with some mild hematuria
Path: alteration in glomerular basement membrane, proliferation of glomerular cells and leukocyte infiltration –> immune complex mediated
Associated with: Hep B and Hep C
Light microscopy: hypercellularity “tram track” from duplication of BM
IF: IgG and C3, C1q and C4
EM: subendothelial electron dense deposits
Course: progresses to RPGN or chronic renal failure

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18
Q

Membranoproliferative glomerulonephritis (Type II)

A

Age: young adults
Clinical: Hematuria, chronic renal failure
Path: dense deposite disease, activation of alternate complement pathway –> autoantibody with hypocomplementemia
Light microscopy: mesangial and endocapillary proliferation, hypercellularity “tram track” from duplication of BM
IF: C3 and IgG
EM: dense deposits in irregular ribbon-like shape
Course: progresses to RPGN or chronic renal failure

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19
Q

Secondary MPGN

A

Age: adults
Clinical: chronic immune complex (SLE, Hep B, Hep C with cryoglobulinemia, endocarditis, HIV, schistosomiasis; alpha 1 antitrypsin; malignant diseases (chronic lymphocytic leukemia and lymphoma); hereditary deficiencies of complement regulatory proteins

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20
Q

IgA Nephropathy (Berger Disease)

A

Age:older children and young adults
Clinical: most common worldwide glomerulonephritis –> recurrent hematuria or proteinuria
Path: prominent IgA deposits in mesangial regions detected by IF
Light microscopy: focal mesangial proliferative glomerulonephritis; mesangial widening
IF: IgA and IgG, IgM and C3 in mesangium
EM: mesangial and paramesangial dense deposits
Course: presents after GI, UTI, strep throat
Prognosis: old age, heavy proteinuria, HTN, glomerulosclerosis lead to worse prognosis

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21
Q

Alport Syndrome

A

Clinical: hematuria with progression to chronic renal failure with deafness and lens dislocation, posterior cataracts and corneal dystrophy
Inherited: x-linked trait mostly, sometimes auto rec or auto dom
Path: abnormal alpha3, alpha4, alpha5 of type IV collagen –> damage to GBM
EM: basket weave appearance
Course: hematuria with red cell casts, proteinuria may develop later

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22
Q

Thin basement membrane lesion (benign familial hematuria)

A

Clinical: familial asymptomatic hematuria and diffuse thinning of GBM
Path: mutations in alpha3 or alpha4 in type IV collagen

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23
Q

Chronic glomerulonephritis

A

Clinical: end stage chronic renal failure
Progression from: crescentic GN, MPGN, IgA nephropathy, FSGS or can occur idiopathic
Light microscopy: cortex is thinned, obliteration of glomeruli, arterial and arteriolar sclerosis
Dialysis changes: arterial intimal thickening, extensive deposition of calcium oxalate crystals in tubules and interstitium, acquired cystic disease
Uremic complications: pericarditis, gastroenteritis, secondary hyperparathyroidism with nephrocalcinosis and renal osteodystrophy, left ventricular hypertrophy
Course: insidiously to renal insufficiency or death from uremia. HTN, cerebral or cardiovascular

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24
Q

Lupus Nephritis

A

recurrent microscopic or gross hematuria, nephritic syndrome, nephrotic syndrome, chronic renal failure, HTN

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25
Q

Henoch-Schonlein Purpura

A

Age: 3-8, adults can occur with serious consequences
Clinical: purpuric skin lesions on extensor arms and legs, buttocks; abd pain with vomiting and intestinal bleeding; ; nonmigratory arthralgia; renal abnormalities; hematuria, nephritic syndrome/ nephrotic syndrome
Light microscopy: mild focal mesangial proliferation or endocapillary to crescentic GN, deposition of IgA with IgG and C3 in mesangial regions
Course: nephrotic, diffuse, crescents have worse prognosis

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26
Q

Bacterial endocarditis - associated GN

A

Clinical: immune complex nephritis from bacterial complexes, hematuria and proteinuria –> RPGN can occur

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27
Q

Diabetic Nephropathy

A

Clinical: Leading causes of chronic kidney failure, nonnephrotic proteinuria, nephrotic syndrome, chronic renal failure
-hyalinizing arteriolar sclerosis
-papillary necrosis, tubular lesions
Light microscopy: capillary basement membrane thickening, diffuse mesangial sclerosis, nodular glomerulosclerosis
Path: metabolic defect with insulin deficiency hyperglycemia, nonenzymatic glycosylation or proteins, hemodynamic changes increasing GFR, increased capillary pressure, glomerular hypertrophy, increased glomerular filtration area
Course: loss of podocytes with apoptosis

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28
Q

Amyloidosis

A

Light chain (AL) or AA type; Congo red-positive fibrillary amyloid deposits in mesangium and capillary walls

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29
Q

Fibrillary glomerulonephritis

A

fibrillar deposits in mesangium and glomerular capillary walls
Clinical: nephrotic syndrome, hematuria, progressive renal insufficiency

30
Q

Immunotactoid glomerulopathy

A

microtubular deposits

31
Q

Microscopic polyangiitis

A

glomerular lesions focal and segmental, necrotizing, glomerulonephritis with hematuria and mild decline in GFR or RPGN

32
Q

Wegener’s granulomatosis

A

c-ANCA

Clinical: crescent formation, mild decline in GFR with hematuria or RPGN with extensive necrosis and fibrin deposition

33
Q

Cryoglobulinemia

A

Deposits of cryoglobulins composed of IgG and IgM complexes
Induces: cutaneous vasculitis, synovitis, proliferative GN typically MPGN
Associated with: Hep C virus and MPGN I

34
Q

Plasma cell dyscrasias (multiple myeloma)

A

circulating monoclonal Ig associated with amyloidosis of light chains, deposition of monoclonal Ig or light chains in GBM, distinctive nodular glomerular lesions
- light chain or monoclonal Ig deposition disease
Present: proteinuria or nephrotic syndrome, HTN, progressive azotemia

35
Q

Acute Kidney Injury/ Acute Tubular Necrosis

A

Clinical: acute diminution of renal function with evidence of tubular injury –> most common cause of acute renal failure
Cause: ischemia from decreased or interrupted blood flow (microscopic polyangiitis, malignant HTN, HUS, TTP, DIC); direct toxic injury to tubules (drugs, radiocontrast dyes, myoglobin, hemoglobin, radiation); acute tubulointerstitial nephritis (hypersensitivity to drugs); urinary obstruction (tumors, BPH, blood clots)
Types: ischemic AKI and nephrotoxic AKI
Path: tubular injury (from depletion of ATP, Ca, proteases, ROS with increased sodium delivery to distal tubules); persistent and severe disturbances in blood flow (hemodynamic alterations causing reduced GFR)
Light microscopy: ischemic –> focal tubular epi necrosis with skip areas, eosinophilic hyaline casts, edema, leukocytes
toxic –> acute tubular injury in PCT
Course: initiation (36 hours), maintenance (sustained decreased urine output to 40-400, oliguria; salt/water; rising BUN; hyperkalemia; metabolic acidosis) and recovery (hypokalemia, increase urine volume, large water/sodium/potassium lost in urine)

36
Q

Tubulointerstitial Nephritis Primary

A

Acute or chronic: acute is rapid with intersitital edema, leukocytic infiltration of interstitium and tubules, focal necrosis
chronic is mono leuk, interstitial fibrosis, tubular atrophy

37
Q

Secondary tubulointerstitial nephritis

A

Examples: polycystic kidney disease, diabetes

38
Q

Acute Pyelonephritis

A

bacterial infection, renal lesion associated with urinary tract infection
Cause: gram negative - E coli, proteus, klebsiella, enterobacter, strep, staph, fungal
Path: hematogenous or ascending from urinary tract
Light microscopy: patchy interstitial suppurative inflammation, intratubular aggregates of neutrophils and tubular necrosis
Complications: papillary necrosis (diabetics and urinary tract obstruction); pyonephrosis (total obstruction so filled with pus); perinephric abscess (suppurative inflammation)
Predisposing: urinary tract obstruction, vesicoureteral reflux, instrumentation, pregnancy, gender and age, preexisting renal lesions, diabetes mellitus, immunosuppression and immunodeficiency

39
Q

Chronic Pyelonephritis

A

bacterial infection dominant with vesicoureteral reflux and obstruction
Path: chronic inflammation and renal scarring with path involvement of calyces and pelvis
- hematogenous or ascending from urinary tract
Cause: gram negative - E coli, proteus, klebsiella, enterobacter, strep, staph, fungal
Types: reflux nephropathy - early in childhood from superimposition of urinary infection on congenital vesicoureteral reflux and intrarenal reflux
chronic obstructive pyelonephritis - recurrent bouts of inflammation and scarring
Light microscopy: irregularly scarred, asymmetric in upper and lower poles
xanthogranulomatous pyelonephritis - accumulation of foamy macrophages mingled with plasma cells, lymph, PMNs, giant cells with proteus
Clinical: HTN, pyuria, bacteriuria, FSGS with proteinuria in nephrotic range

40
Q

Acute Drug-Induced Interstitial Nephritis

A

Causes: sulfonamides, penicillins, rifampin, diuretics (thiazide), NSAIDS, allopurinol and cimetidine
Path: begins 15 days after exposure to drug
- late phase reaction IgE mediated (type I) hypersensitivity or T cell mediated delayed hypersensitivity reaction (type IV)
Clinical: fever, eosinophilia, rash, renal abnormalities (hematuria, proteinuria, leukocyturia with eosinophils), rising creatinine or acute renal failure with oliguria
Light microscopy: eosinophils and neutrophils, plasma cells, basophils, interstitial non-necrotizing granulomas with giant cells

41
Q

Analgesic Nephropathy

A

Gender: women more than men
Clinical: chronic renal disease caused by excessive intake of analgesic mixtures
Path: chronic tubulointerstitial nephritis and renal papillary necrosis –> papillary necrosis first with cortical tubulointerstitial nephritis follows from impeded urine outflow
Cause: aspirin, caffeine, acetaminophen, codeine, phenacetin
Light microscopy: Various stages of necrosis
Course: headaches, muscle pain, psychosis, hyposthenuria, anemia, GI, HTN
- resolves after drug withdrawal or develop into transitional papillary carcinoma of renal pelvis

42
Q

Nephropathy Associated with NSAIDs

A

Path: from inhibition of cyclooxygenase prostaglandin synthesis
Diseases: acute renal failure, acute hypersensitivity interstitial nephritis, acute interstitial nephritis and minimal change disease, membranous nephropathy

43
Q

Aristolochic Nephropathy

A

Herbal remedies leading to chronic tubulointerstitial nephritis –> renal failure and interstitial fibrosis with paucity of infiltrating leukocytes

44
Q

Urate Nephropathy

A

Hyperuricemia can lead to: acute uric acid nephropathy (obstruction of nephrons and acute renal failure); chronic urate nephropathy (birefringent needle-like crystals in tubular lumens or interstitium leading to a tophus with renal arterial and arteriolar thickening); nephrolithiasis

45
Q

Hypercalcemia

A

Caused: hyperparathyroidism, multiple myeloma, vit D intoxication, metastatic CA, excess calcium intake

46
Q

Acute Phosphate Nephropathy

A

Calcium phosphate crystals in tubules from phosphate solutions for colonoscopy –> excess phosphate

47
Q

Light Chain Cast Nephropathy

A

Tubulointerstitial from complications of tumor (paraneoplastic syndromes) or therapy (radiation) in addition to Multiple Myeloma
Path: Bence Jones proteinuria and cast nephropathy; amyloidosis of AL; light chain deposition disease in GBM and mesangium; hypercalcemia and hyperuricemia
Light microscopy: light chain casts pink to blue
Clinical: Chronic renal failure or acute renal failure with oliguria

48
Q

Benign Nephrosclerosis

A

Clinical: sclerosis of renal arterioles and small arteries –> focal ischemia of parenchyma with narrowed lumen
Path: medial and intimal thickening from hemodynamic changes, aging, genetic defects; hyaline deposition in arterioles
Gross: cortical scarring and shrinking with fine even granularity
Light microscopy: narrowing of arterioles and small arteries from hyalinization of walls and thickening with fibroelastic hyperplasia
- pathcy ischemic atrophy
Course: very small amount of manifestations
- reduced renal blood flow, GFR normal, mild proteinuria
- if have associated HTN worse prognosis

49
Q

Malignant Hypertension

A

Age: young black men
Clinical: Accelerated hypertension
Path: vascular damage to the kidneys with increased permeability of small vessels to fibrinogen and plasma proteins, endo injury, focal death of cells –> fibrinoid necrosis of arterioles and small arteries with swelling of vascular intima and intravascular thrombosis
- elevated levels of plasma renin, markedly ischemic
Gross: flea bitten appearance
Light microscopy: fibrinoid necrosis of arterioles with eosinophilic granular change in BV wall
- hyperplastic arteriolitis with onion skin lesion
Course: BP above 200 mmHg and diastolic pressures above 120 mmHg, papilledema, retinal hemorrhages, encephalopathy, CV abnormalities, renal failure
- marked proteinuria or microscopic hematuria

50
Q

Renal Artery Stenosis

A

Clinical: unilateral renal artery stenosis causes HTN
- elevated plasma or renal vein renin levels
Caused: occlusion by atheromatous plaque more frequently in men or fibromuscular dysplasia of renal artery which is more common in women
Light microscopy: arteriolosclerosis
Course: good prognosis after surgery

51
Q

Typical HUS

A

Age: usually children
Clinical: microangiopathic hemolytic anemia, thrombocytopenia, renal failure –> hematemesis and melena, oliguria, hematuria, neuro changes possibly HTN
Cause: E. coli with shigalike toxins
Path: endothelial injury mostly, platelet activation and aggregation
Light microscopy: thrombotic lesions in capillaries and arterioles; schistocytes in blood smears –> patchy diffuse cortical necrosis with thrombi, hypercellular with thickening and splitting of BM
Course: good prognosis if treated early

52
Q

Atypical HUS

A

Age: adults
Clinical: microangiopathic hemolytic anemia, thrombocytopenia, renal failure
Cause: inherited complement factor H deficiency, factor I and CD46 deficiency
-antiphospholipid syndrome, postpartum renal failure, vascular diseases affecting kidney, chemo/immunosuppressive drugs, irradiation of kidney
Path: endothelial injury mostly, platelet activation and aggregation
Light microscopy: thrombotic lesions in capillaries and arterioles; schistocytes in blood smears –> patchy diffuse cortical necrosis with thrombi, hypercellular with thickening and splitting of BM
Course: not good prognosis, can turn chronic

53
Q

TTP

A

Clinical: microangiopathic hemolytic anemia, thrombocytopenia, renal failure –> CNS involvement
Cause: defect in ADAMTS13
Path: endothelial injury, platelet activation and aggregation mostly
Light microscopy: thrombotic lesions in capillaries and arterioles; schistocytes in blood smears –> patchy diffuse cortical necrosis with thrombi, hypercellular with thickening and splitting of BM
Course: not good prognosis, can turn chronic

54
Q

Sicke Cell Disease Nephropathy

A

hematuria and diminished concentrating ability with papillary necrosis and proteinuria

55
Q

Diffuse cortical necrosis

A

condition after OB emergency, septic shock, extensive surgery
Light microscopy: ischemic necrosis with microthrombi

56
Q

Renal Infarcts

A

End organ nature of blood with limited collateral circulation from extrarenal sites –> infarct from embolism

  • white renal infarcts, 24 hours sharply demarcated pale yellow-white areas
  • wedge-shaped infarct
57
Q

Hypoplasia

A

No scars, reduced number of renal lobes and pyramids –> usually 6 or fewer

58
Q

Adult polycystic kidney disease

A

Inheritance: auto dom
Path: large multicystic kidneys, liver cysts, berry aneurysms
Clinical: hematuria, flank pain, UTI, renal stones, HTN
Outcome: chronic renal failure beginning at 40-60 years
Extra: multiple expanding cysts of both kidneys destroying renal parencyma and cause renal failure
- mutation of PKD gene; PKD1 (polycystin1) and PKD2 (polycystin 2)
- genes located on primary cilium which affects Ca
- leads to cellular proliferation, apoptosis, interactions with ECM
Gross: large size, cysts enlarge on calyces and pelvis
Extrarenal: cysts in liver too, berry aneurysm, mitral valve prolapse

59
Q

Childhood polycystic kidney disease

A

Age: perinatal, neonatal, infantile, juvenile
Inheritance: auto recessive
Path: enlarged cystic kidneys at birth
Clinical features: hepatic fibrosis
Outcome: variable, death in infancy or childhood
Mutations: PKHD1 which causes fibrocystin
Gross: spongy kidney with small cysts in cortex and medulla

60
Q

Medullary sponge kidney

A

Age: adult
Inheritance: none
Path: medullary cysts on excretory urography
Clinical: hematuria, UTI, recurrent renal stones
Outcome: benign
Extra: lesions consisting of multiple cystic dilations of collecting ducts in medulla

61
Q

Familial juvenile nephronophthisis

A

Inheritance: auto rec
Path: corticomedullary cysts, shrunken kidneys
Clinical: salt wasting, polyuria, growth retardation, anemia
Outcome: progressive renal failure beginning in childhood
Extra: cysts in medulla concentrated at corticomedullary junction
-present with polyuria and polydipsia without being able to concentrate renal tubules
- NPH1-3 present in primary cilia
Gross: cysts in medulla

62
Q

Adult-onset medullary cystic disease

A

Inheritance: auto dom
Path: corticomedullary cysts, shrunken kidneys
Clinical: salt wasting, polyuria
Outcome: chronic renal failure beginning in adulthood
Gross: cysts in medulla

63
Q

Simple cysts

A 
Inheritance: none
Path: single or multiple cysts in normal sized kidneys
Clinical: micrscopic hematuria
Outcome: benign
- No clinical significance
64
Q

Acquired renal cystic disease

A

Inheritance: none
Path: cystic degeneration in end stage kidney disease
Clinical: hemorrhage, erythrocytosis, neoplasia
Outcome: dependence on dialysis
- most asymptomatic cysts but can bleed or cause renal cell CA

65
Q

Hydronephrosis

A

dilation of renal pelvis and calyces associated with progressive atrophy of kidney due to obstruction

  • can lead to interstitial fibrosis
  • decreased glomerular filtration rate
66
Q

Urolithiasis

A

Causes: calcium stones, triple stones or struvite stones (Mg Ammonium phosph), uric acid stones, cystine
Path: 1. hypercalcemia and hypercalciuria leads to calcium stones
2. Mg ammonium phosphate stones formed by infections of bacteria (proteus and staph) –> staghorn calculi
3. uric acid stones –> from gout or unknown
4. cystine stones from genetic defects

67
Q

Renal Papillary Adenoma

A

Small adenomas from renal tubular epithelium
Gross: pale yellow-gray discrete well-circumscribed nodules
Light microscopy: branching papillomatous structures with complexity

68
Q

Renal Cell Carcinoma

A

Most common malignant tumor
- yellow color resemble tumor cells or clear cells
Risk factor: tobacco, obesity, HTN, estrogen, asbestos, heavy metals, chronic renal failure, acquired cystic disease
- VHL syndrome associated, hereditary clear cell CA, papillary CA
Path: 1. clear cell carcinoma most common type - VHL related
2. papillary carcinoma with trisomies 7.16, 17, hepatocyte growth factor –> DCT, associated with dialysis, cuboidal columnar cells with foam cells and psammoma bodies
3. chromophobe renal carcinoma –> pale cells with perinuclear halo
4. Collecting duct carcinoma - rare with nests of malignant cells
Presentation: costovertebral pain, palpable mass, hematuria or constitutional symptoms
Paraneoplastic: polycythemia, hypercalcemia, HTN, hepatic dysfunction, feminization or masculinization, cushing syndrome, eosinophilia, leukemoid reactions, amyloidosis
Prognosis: metastasize

69
Q

Wilms Tumor

A

Most common malignant tumor in children, mixed tumors

70
Q

Angiomyolipoma

A

Tumor consisting of vessels, smooth muscle, fat

- occurs with tuberous sclerosis (caused by loss of function TSC1 or TSC2 tumor suppressor genes)

71
Q

Oncocytoma

A

Epithelial tumor with large eosinophilic cells with small round benign appearing nuclei with large nucleoli
- numerous mitochondria

Pathology (12 decks)

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