Renal

Question 1

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

Answer 1

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

Question 2

Renal insufficiency (GFR, BUN, creatinine, presentation)

Answer 2

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

Question 3

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

Answer 3

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

Question 4

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

Answer 4

GFR < 5%, terminal stage of uremia

Question 5

Nephritic syndrome

Answer 5

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

Question 6

Nephrotic syndrome

Answer 6

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

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

Question 7

Poststreptococcal Postinfectious Glomerulonephritis (acute proliferative)

Answer 7

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

Question 8

Nonstreptococcal acute glomerulonephritis

Answer 8

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

Question 9

Rapidly progressive glomerulonephritis

Answer 9

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

Question 10

Goodpasture’s syndrome

Answer 10

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

Question 11

Type II RPGN

Answer 11

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

Question 12

Type III RPGN

Answer 12

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

Question 13

Membranous nephropathy

Answer 13

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

Question 14

Minimal change disease

Answer 14

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

Question 15

Focal segmental glomerulosclerosis

Answer 15

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

Question 16

HIV associated nephropathy

Answer 16

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

Question 17

Membranoproliferative glomerulonephritis (Type I)

Answer 17

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

Question 18

Membranoproliferative glomerulonephritis (Type II)

Answer 18

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

Question 19

Secondary MPGN

Answer 19

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

Question 20

IgA Nephropathy (Berger Disease)

Answer 20

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

Question 21

Alport Syndrome

Answer 21

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

Question 22

Thin basement membrane lesion (benign familial hematuria)

Answer 22

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

Question 23

Chronic glomerulonephritis

Answer 23

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

Question 24

Lupus Nephritis

Answer 24

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

Question 25

Henoch-Schonlein Purpura

Answer 25

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

Question 26

Bacterial endocarditis - associated GN

Answer 26

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

Question 27

Diabetic Nephropathy

Answer 27

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

Question 28

Amyloidosis

Answer 28

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

Question 29

Fibrillary glomerulonephritis

Answer 29

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

Question 30

Immunotactoid glomerulopathy

Answer 30

microtubular deposits

Question 31

Microscopic polyangiitis

Answer 31

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

Question 32

Wegener's granulomatosis

Answer 32

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

Question 33

Cryoglobulinemia

Answer 33

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

Question 34

Plasma cell dyscrasias (multiple myeloma)

Answer 34

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

Question 35

Acute Kidney Injury/ Acute Tubular Necrosis

Answer 35

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)

Question 36

Tubulointerstitial Nephritis Primary

Answer 36

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

Question 37

Secondary tubulointerstitial nephritis

Answer 37

Examples: polycystic kidney disease, diabetes

Question 38

Acute Pyelonephritis

Answer 38

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

Question 39

Chronic Pyelonephritis

Answer 39

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

Question 40

Acute Drug-Induced Interstitial Nephritis

Answer 40

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

Question 41

Analgesic Nephropathy

Answer 41

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

Question 42

Nephropathy Associated with NSAIDs

Answer 42

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

Question 43

Aristolochic Nephropathy

Answer 43

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

Question 44

Urate Nephropathy

Answer 44

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

Question 45

Hypercalcemia

Answer 45

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

Question 46

Acute Phosphate Nephropathy

Answer 46

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

Question 47

Light Chain Cast Nephropathy

Answer 47

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

Question 48

Benign Nephrosclerosis

Answer 48

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

Question 49

Malignant Hypertension

Answer 49

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

Question 50

Renal Artery Stenosis

Answer 50

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

Question 51

Typical HUS

Answer 51

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

Question 52

Atypical HUS

Answer 52

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

Question 53

TTP

Answer 53

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

Question 54

Sicke Cell Disease Nephropathy

Answer 54

hematuria and diminished concentrating ability with papillary necrosis and proteinuria

Question 55

Diffuse cortical necrosis

Answer 55

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

Question 56

Renal Infarcts

Answer 56

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

Question 57

Hypoplasia

Answer 57

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

Question 58

Adult polycystic kidney disease

Answer 58

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

Question 59

Childhood polycystic kidney disease

Answer 59

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

Question 60

Medullary sponge kidney

Answer 60

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

Question 61

Familial juvenile nephronophthisis

Answer 61

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

Question 62

Adult-onset medullary cystic disease

Answer 62

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

Question 63

Simple cysts

Answer 63

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

Question 64

Acquired renal cystic disease

Answer 64

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

Question 65

Hydronephrosis

Answer 65

dilation of renal pelvis and calyces associated with progressive atrophy of kidney due to obstruction - can lead to interstitial fibrosis - decreased glomerular filtration rate

Question 66

Urolithiasis

Answer 66

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

Question 67

Renal Papillary Adenoma

Answer 67

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

Question 68

Renal Cell Carcinoma

Answer 68

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

Question 69

Wilms Tumor

Answer 69

Most common malignant tumor in children, mixed tumors

Question 70

Angiomyolipoma

Answer 70

Tumor consisting of vessels, smooth muscle, fat | - occurs with tuberous sclerosis (caused by loss of function TSC1 or TSC2 tumor suppressor genes)

Question 71

Oncocytoma

Answer 71

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