Kidney Flashcards
average wt adult of kidney
150 g
lower urinary tract division
pelvicalcyceal system
ureters
bladder
urethra
cortical thickness of normal kidney
1-1.5 c,
elevation of BUN and creatinine levels
decreased GFR
azotemia
prerenal azotemia
hypoperfusion of kidneys that impairs renal fxn without parenchymal damage
postrenal azotemia
obstruction beyond the level of the kidney
failure of renal excretory function
metabolic and endocrine alterations resulting from renal damage
uremia
classic presentation of acute poststreptococcal GN
nephritic syndrome
nephritic syndrome signs
acute onset of grossly visible hematuria mild to mod proteinuria azotemia oliguria edema hytpertension
nephritic syndrome with rapid decline - hours to days
RPGN
nephrotic syndrome signs
heavy proteinuria >3.5 g/day hypoalbuminemia severe edema hyperlipidemia lipiduria
acute renal failure
oliguria or anuria
recent onset of azotemia- acute tubular necrosis
renal tubular defects
polyuria
nocturia
electrolyte dsorders
renal tubular defect cause
dse that directly affect tubular structure
or
cause defects in tubular functions
urinary tract infection
bacteriuria
pyuria
symptomatic or not
kidney uti
pyelonephritis
bladder uti
cystitis
nephrolothiasis
severe spasms of pain
hematuria
recurrent stone formation
end result of all renal parenchymal diseases
chronic renal failure
cause of chronic renal failure
azotemia -> uremia
chronic
stage 1
DIMINISHED RENAL RESERVE
GFR 50%
normal serum BUN and creatine
asymptomatic
susceptible to azotemia with additional renal insult
stage 2
RENAL INSUFFICIENCY
GFR 20-50% azotemia anemia hypertension polyuria nocturia uremia precepitated by stress
stage 3
CHRONIC RENAL FAILURE
<20-25% GFR edema metabolic acidosis hyperkalemia overt uremia dneuroooig GI CV complications
stage 4
END STAGE RENAL DISEASE
<5% GFR
terminal stage of uremia
systemic manifestations:
FLUID AND ELECTROLYTES
metabolic acidosis
edema
hyperkalemia
dehydration
systemic manifestations:
CALCIUM
PHOSPHATE
BONE
hyperphosphatemia
secondary hyperparathyroidism
hypocalcemia
renal osteodystrophy
systemic manifestations:
HEMATOLOGIC
anemia
bleeding diathesis
systemic manifestations:
CARDIOPULMONARY
cardiomyopathy congestive heart failure hypertension uremic pericarditis pulmonary edema
gastrointestinal manifestations
bleeding esophagitis gastritis colitis nausea vomiting
systemic manifestations
NEUROMUSCULAR
peripheral neuropathy
encephalopathy
myopathy
systemic manifestations
DERMATOLOGIC
pruritus
sallow color
dermatitis
cavity in which plasma filtrate collects first
urinary space
supporting network of the interconnecting capillary lumen
mesangium
glomerulus fxn
maintain the integrity of the glomerular filtration barrier
glomerular filtration barrier composition
fenestrated endothelial cells
basement membrane
epithelial podocytes layer or visceral layer
factors that determine filtration
size of the molecule
charge of the barrier
MW of molecules that can pass through the filter
<70 kilodalton
responsible for the slit like diaphragm
podocytes or visceral epithelium
charge of the barrier
anionic
charge of the substance
cationic
coats the membranes of endothelial and epithelial together with the basement membrane
responsible for the negative charge of the barrier
proteoglycans
sialoglycans
increase in number of cells in the glomerular tufts
hypercellularity
hypercellulariy characteristics
cellular proliferation of mesangial, endothelial, epithelial cells
leukocytic infiltration of neutrophils, monocytes, lymphocytes
crescents
composition of crescents
parietal epithelial cells
leukocytes
elicits crescenteric response
fibrin
basement membrane thickening is due to deposition of
immune complexes on the endothelial and epithelial side of the basement membrane or within GBM itself
hyalinosis denotes accumulation of
plasma proteins as a consequence of capijllary or endothelial wall injury
sclerosis is accumulations of
extracellular collagenous matrix in mesangial areas and or capillary loops
common feature of focal segmental glomerulosclerosis
hyalinosis
capillary lumen obliteration by sclerosis could lead to formation of
fibrous adhesions between the sclerotic portions of the glomeruli and the nearby parietal epithelium
hyalinosis and sclerosis are manifestations of
end stage irreversible injury
numerous discrete electron-dense deposits along the subepithelial aspect of the basement membrane
granular pattern
Heymann Nephritis
Heymann antigen with homology to LDL receptor
megalin
immune mechanism which includes cationic molecules that bind to anionic components of the glomerulus
DNA, nucleosomes, and other nuclear proteins, bacterial products, etc
granular pattern
antibodies against planted antigens
antibodies are directed against intrinsic fixed antigens that are normal components of the GBM
diffuse linear pattern
anti GBM antibody induced GN
anti GBM cross react to lung alveoli, a feature of
Goodpasture Syndrome
GBM antigen responsible for classic anti GBM GN and Goodpature syndrome is a component of
NC1 of the alpha 3 chain of collagen type 4
fxn of NC1 of the alpha 3 chain of collagen type 4
maintenance of GBM suprastructure
anti GBM GN are characterized by —- and the clinical syndrome of —–
severe cresenteric glomerular damage
RPGN
caused by trapping of circulating ag ab complex
granular
circulating immune complex GN
endogenous origin of antigens that trigger circulating immune complexes
SLE
exogenous origin of antigens that trigger circulating immune complexes
hepa b, c
treponema
plasmodium
tumor
continuous cycles of immune complex formation as seen in SLE and viral hepatitis may lead to
membranous or membranoproliferative type of GN
alternative complement pathway activation occurs in
dense deposit disease
MPGN type 2
-may occur in some proliferative GN
epithelial cell injury is seen in
minimal change disease
focal segmental glomerulosclerosis
Primary glomerular diseases under acute nephritis
acute diffuse GN
rapid progressive/crescentic GN
Primary glomerular diseases under nephrotic presentation
minimal change disease
focal segemental glomerulosclerosis
membranous GN
membranoproliferative GN
Primary glomerular diseases under primary hematuria
IgA nephropathy or Berger’s dse
prototype of acute diffuse glomerulonephritis
Poststrep GN
histologic alterations in acute diffuse GN
hypercellularity
features of acute diffuse GN
1-4 weeks after strep infection 6-10 years old hematuria, edema, HTN can be endogenous or exogenous GRANULAR
etiologic agent of acute diffuse GN
nephritogenic strains of group A- beta hemolytic strep types 12,14,1
pathogenesis of acute diffuse GN
circulating ab-ag complexes➡️entrapped in glomeruli➡️glomerular injury by activation of complement by immune complexes
deposited in the GBM and mesangium in acute diffuse GN
IgG
IgM
C3
electron microscopy feature of acute diffuse Gn
discrete amorphous electron dense deposit on the epithelial side of the membrane
HUMPS
clinical course of acute diffuse GN
good prognosis
young child develops malaise, fever, nausea, oliguria, hematuria
other postinfectious GN
staphylococcal endocarditis pneumococcal pneumonia meningococcemia hep b,c varicella hiv infectious mononucleosis malaria toxoplasmosis
severe proliferation that obliterates the glomerular tuft resulting to rapid and progressive decline
rapid progressive GN
manifestation of RPGN
severe olioguria
nephritis
crescent formation
3 groups based on immuno mechanism RPGN
1: anti GBM antibody induced ( renal limited)
2: immune complex mediates
3: pauci-immune type
syndrome associated with type 1 RPGN
Goodpasture syndrome
pattern of IgG and C3 deposition
linear
complication of post infectious GN, lupus nephritis, henoch-schonlein purpura
granular pattern
type 2 immune complex mediated
has circulating ANCAs which attacks visceral epithelial cells
type 3: pauci immune type
RPGN gross morphology
enlarged, pale, with cortical petechial hemorrhage
RPGN light microscopy features
crescent formation by proliferation of parietal epithelial cells
obliterated bowman’s space
WBC migration and some fibrin strands between crescent layers
electron microscopy RPGN features
subepithelial deposits and rupture of the GBM
cause fibrin to escape the glomerulus and settle in space
manifestations of nephrotic syndrome
massive proteinuria hypoalbuminemia generalized edema hyperlipidemia lipiduria
most important primary glomerular dse
primary: children: lipoid nephrosis
secondary: adults: membranous GN
all ages: focal segmental GS
may occur with lipiduria in patients susceptible to infection
globinuria
loss of anticoagulant glycoprotein factors in patients with nephrotic syndrome may lead to
thrombotic or thromboembolic complications
most common nephrotic syndrome in adults
membranous GN
membranous GN histological features
uniform diffuse thickening of capillary walls
irregular SPIKES of silver staining matrix
effaced foot processes
pathogenesis of membranous GN
direct action of c5-c9 which activates the glomerular mesangial and epithelial cells ➡️liberates proteases and oXidants➡️capillary wall injury➡️increased protein leakage
most common type of membranous GN 85%
idioipathic or primary
2ary membranous GN etiologies
hep b, c
penicillamine, captopril, gold therapy, NSAIDs
lung ca, colon, melanomas
SLE 15%
clinical course of membranous GN
40% of cases can proceed to renal failure adults nonselective proteinuria poor response to corticosteroid therapy sudden presentation, minimal hematuria
most frequent cause of nephrotic syndrome in children
minimal change disease or lipoid nephrosis
most characteristic feature of minimal change disease
good response to corticosteroid therapy
pathogenesis of minimal change disease
abscence of immune complexes
elaboration of cytokine (t cell derived)like circulating substance leads to proteinuria
proteinuria selective to albumin only
light microscopy feature of minimal change disease
normal
immunofluorescence feature of minimal change dse
normal, no deposits
electron microscopy feature of minimal change disease
uniform and diffuse foot processes replaced by a rim of cytoplasm often showing vacuolization, swelling, and hyperplasia of villi
MCD in adults is associated with
Hodgkin’s lymphoma
secondary MCD may follow
NSAID therapy
associated with acute interstitial nephritis
most common form of glomerulosclerosis in adults
focal segmental GS
hallmark of FSFGS
epithelial damage
pathogenesis of FSGS
epithelial damage
hyalinosis
sclerosis
on LM, FSGS initially involves only
juxtamedullary glomeruli
immunoflorEscence features of FSGS
deposition of IgM and c3 in sclerotic areas and or mesangium
FSGS may lead to
global glomerulosclerosis with pronouced tubular atrophy and interstitial fibrosis
morphologic variant of FSGs
collapsing glomerulopathy
cause of collapsing glomerulopathy
idiopathic but is the most characteristic lesion of HIV associated nephropathy
clinical course of FSGS
poor corticosteroid response
clincal presentation: nephrotic or mixed nephrotic/nephritic with low c3
MPGN or mesangiocapillary GN
idiopathic type 1 MPGN
immune complexes in the glomerulus
activation of both classic and alternative pathways
type 2 MPGN or dense deposit dse
activation of alternative complement pathway
consistently decreased serum c3 but normal c4 and c1
low factor b and properdin
no IgG deposition
C3NeF
secondary MPGN
SLE, hep b,c
alpha 1-antitrypsin deficiency
CLL, lymphoma
hereditary deficiency of complement regulatory proteins
MPGN morphology
segmental basement membrane thickening proliferation enlarged glomeruli leukcytic infiltration double track or SPLITTING in pas or silver stain
GBM thickening of MPGN is at
peripheral capillary loops
type 1 MPGN
subendothelial electron dense deposits
c3 deposited in GRANULAR pattern
IgG and early complement proteins(c1q and 4)
type 2 MPGN
lamina densa becomes irregular, ribbonlike
c3 in irregular granular or linear foci in BM on either side
c3 in mesangium : MESANGIAL rings
no IgG
frequent cause of recurrent gross hematuria and mild proteinuria
immunoflorEscence microscopy detection only
IgA nephropathy or Berger disease
IgAN epidemiology
most common form of GN except among African americans
bad prognosis in IgAN
> 1g/day
HTN
pathogenesis of IgAN
IgA links with antigen and is carried into circulation➡️deposition in mesangium➡️activates complement➡️injury
morphology of IgAN
mesangial deposition of IgA with c3, properdin and lesser amts of IgG and IgM
c1q, 4 absent
treatment for IgAN
ACE inh
ARBs
renal transplantation for recurrent cases
2 hereditary nephritis
alport syndrome
thin basement membrane dse
clinical features of aliport syndrome
hematuria progressing to renal failure
nerve deafness
various eye disorders
mode of inheritance of Alport syndrome
X linked
pathogenesis of alport syndrome
mutation of gene encoding TYPE 4 collagen
- GBM, lens of the eye, cochlea
morphology of alport syndrome
basket weave appearance
- irregular foci of thickening and alternating with attenuation (thinning)
- pronounced splitting and lamination of the lamina densa
aka BENIGN FAMILIAR HYPERPLASIA
thin membrane disease
clinical manifestation of TBMD
familial asymptomatic hematuria discovered on urine urinalysis
GBM is thinned frm 300-400mm normal to
150-250mm
mode of inheritance of TBMD
heterozygous
pathogenesis of TBMD
defective genes encoding alpha 3 or alpha 4 chains of type 4 collagen
gross Chronic GN
symmetrically contracted
diffusely granular cortical surface
thinned out cortex
increased pelvic fat
progression sign in chronic GN
obliteration of glomeruli➡️acellular eosinophilic masses
potential etiologic factors of SLE
EBV
estrogen
HLA b???
procainamide
seen in 5%’SLE patients
class 1 minimal or no detectable abnormality
seen in 10-25% SLE patients
granular mesangial deposits of IG and complement
class 2 mesangial lupus glomerulonephritis
20-25% of SLE patients
class 3 focal proliferative glomerulonephritis
most serious form of Lupus nephritis
class 4 diffuse proliferative GN
wire loop due to capillary basement membrane thickening
diffuse proliferativ GN
similar to idipathic GN
class 5 membranous GN
one of the most common cause of end stage renal failure
diabetic nephropathy
diabetes can affect the kidney in 3 forms
complications of diabetic vasculature
diabetic glomerular damage
increased susceptibility to infection and papillary necrosis
contributors to renal tissue injury
hyperglycemia
non enzymatic glycosylation of proteins
hemodynamic changes
morphologic changes in diabetic nephropathy
capillary BM thickening
diffuse messangial sclerosis
nodular sclerosis- Kimmelstiel Wilson disease
purpuric skin lesions affecting the extensor surface of arms, legs, buttocks
abdominal manifestation
urinary abnormalities
poor prognosisi for adults
henodch schonlein
renal manifestations of HS
gross or microscopic hematuria
proteinuria
nephrotic syndrome
documents amyloidosis
congo red stain
amyloid deposition in kidneys
GBM
mesangium
resemble amyloid fibrils but does not stain with Congo red
Fibrillary GN
deposits are microtubular in structure and 30-50 nm in width
immunotactoid GN
main causes of tubular injury
ischemia
aka acute tubular necrosis
acute tubular injury
most common cause of acute renal failure
acute kidney injury
mechanism of AKI
failure to maintain fluid and electrolyte, and acid base balance manifesting as oliguria or urine flow to less than 400mL within 24 hours
part most susceptible to ischemia
proximal convoluted tubule
toxic substances to tubules
gentamycin radiocontrast dyes myoglobin hemoglobin radiation
2 patterns of AKI based on process involved
ishemic
nephrotoxic
two events in AKI
disturbance in blood flow
injury to tubuloepithelial cell
acute tubular necrosis morphology
karyolytic necrotic tubular cells
focal, patchy
coagulative necrosis
separation of cells from BM- tuborerrhexis
AKI initiation phase
- 36 hours
slight decrease in urine output
rise in BUN / creatinine
AKI maintenance phase
sustained decrease in urine output (40-400ml a day rising BUN and creatinine hyperkalemia metabolic acidosis uremia
recovery phase of aki
Increae urine output to 3L per day with water
sodium and potassium losses
renal tubule function restored
hypokalemia becomes a concern
distinguished from glomerular diseases by the absence of the hallmarks of nephritic or nephrotic syndrome
tubuluinterstitial nephritis
most common cause of tubulointerstitial nephritis
infections
metabolic causes of interstitial nephritis
urates
calcium
oxalates
acute form of tubulointerstitial nephritis
neutrophils and eosinophils
edema of the interstitium
chronic form of tubulointerstitial nephritis
lymphocytes, plasma cells
interstitial fibrosis
tubular atrophy
pyelonephritis affects
tubules
interstitium
renal pelvis
dominant etiologic agents of pyelonephritis
E.coli
Proteus
Klebsiella
Enterobacter
viral etiologic agents of pyelonephritis
polyoma virus
cmv
adenovirus
2 routes in pyelonephritis
ascending
hematogenous
hematogenous route results from seeding bacteria from
septicemia
infective endocarditis
type of inflammation in actue pyelonephritis
diffuse suppurative
acute pyelonephritis complication seen in diabetics and bilateral ut obstruction
papilary necrosis
complication of acute pyelonephritis due to total or almost complete obstruction high in the urinary tract
pyonephrosis
complication of acute pyelonephritis
extension into the renal capsule and perinephric tissue
perinephric abscess
classic symptoms of acute pyelonephritis
fever costovertebral lumbar tenderness pain dysuria pyuria
gross hallmark of chronic pyelonephritis
pitting geographic scars
most common mechanism in acquiring chronic pyelonephritis
reflux due to anatomic defect in the valve
reflux leads to
reflux nephropathy
in this mechanism the pressure is reflected backwards causing dilatation to the helices
obstructive
in reflux nephropathy, injury is at the
upper and lower poles of kidney
in chronic obstructive nephropathy, injury is
distributed in all areas
chronic pyelonephritis microscopic features
mononuclear inflammation
interstitial fibrosis
tubular atrophy- flattened epithelium
thyroidization
three ways in which drugs or toxins produce renal injury
intersitial immunological reaction
acute renal failure
cumulative injury
acute drug induced interstitial nephritis is associated with
penicillins rifampin diuretics nsaids allopurinol cimetidine
sulfonamide
acute drug induced interstitial nephritis begins
after 2 weeks of exposure
mechanism of acute drug induced interstitial nephritis
type 1 hypersensitivity reaction because of eosinophilia and elevated serum IgE levels
chronic disorder due to excessive intake of
aspirin
tylenol
nsaids
analgesic nephropathy
analgesics contain this substance which depletes tubular cells of glutathione and then induce the formation of oxidative metabollites
phenacetin
morphological characteristics of analgesic nephropathy
q
papillary necrosis
chronic tubulointerstital nephritis
clinical features of acute drug induced interstitial nephritis
women
those with recurrent headache, muscle pain, psychoneurotic patients and factory workers
UTI complicatesn50% of cases
small % pose a risk in developing transitional carcinoma of the renal pelvis
precipitiation of urate crystals in the tubules like
low pH
3 clinical forms of urate nephropathy
acute urate nephropathy
chronic urate or gouty nephropathy
urate nephrolithiasis
usually seen in patients with leukemias and lymphomas
acute urate nephropathy
genetic disposition of the individual to hyperuricemia
chronic urate nephropathy
uric acid in kidney is in its ionized form which precipitates in the tubules especially in acidic environment
urate nephrolithiasis
caused by complications of nonrenal malignant tumors of hematopoietic origin and therapy
multiple myeloma
light-chain cast nephropathy
causes direct toxicity to tubules and forms a cast giving rise to tubular obstruction
bence jonce protein
aka arteriolar nephrosclerosis
benign nephrosclerosis
benigh NS affects
renal arterioles and small arteries
benign NS is associated with
low grade essential HTN
DM
at risk groups of developin renal insufficiency in benign NS
african descent
more severe BP elevations
second underlying disease
gross feature of benign NS
grain leather appearance
loss of mass
histologic features of bening NS
arteriolar thickening and hyalinization
fibroplastic hyperplasia of interlobular and arcuate aa.
associated with rapidly progressive or accelerated HTN
malignant NS
gross features of malignant NS
kidney size depends on the duration and severity
small pinpoint petechial hemorrhages on cortical surface
histologic features of malignant ns
vascular damage fibrinoid necrosis onion skinning ischemia significant luminal narrowing
rare cause of kidney hypertension caused by renin secretion by cells of the JG apparatus
renal artery stenosis
pathologic lesions of renal artery stenosis
atheromatous plaque
fibromuscular dysplasia type
more common cause of renal artery stenosis
atheromatous plaque
fibromuscular, dysplasia type of lesion in renal artery stenosis is seen in
women and younger age groups
constriction in fibromuscular lesion of renal stenosis is usually at
middle or distal portion of the renal artery
fibroproliferation or nonatherosclerotic hyperplasia is most common in
medial hyperplasia
clinical features of renal artery stenosis
essential HTN similarities
bruit on auscultation of kidneys
arteriography required
special stain in fibromuscular dysplasia renal stenosis
elastin stain
characterized clinically by microangiopathic hemolytic anemia, thrombocytopenia, renal failure
thrombotic microangiopathies
important clue in the diagnosis of TMA
schistocutes
morphological lesion in TMA
thrombotic lesions in capillaries and arterioles
hemolytic uremic syndrome is largely due to
endothelial injury
TTP is largely due to
platelet activation
typical HUS
epidemic, classic, diarrhea postive
Typical HUS is associated with infection of
E coli strains O157:H7
producing shiga-like toxin
atypical HUS is associated with inherited deficiency or mutation of complement regulatory proteins
atypical, nonepidemic, diarrhea negative HUS
c3 regulatory proteins function
inactivates c3 convertase in order to oppose the action od rhe alternative complement pathway
acquired causes of endothelial injury in atypical HUs
antiphospholipid antibodies pregnancy complications oral contraceptives vascular renal diseases such as scleroderma and hypertensions chemo and immunosup drugs radiation
deficiency in TTP
ADAMTS13
ADAMTS13 function
metalloprotease the regulates the function of the vWF
gross features of thrombotic microangiopathy
patchy or diffuse cortical necrosis and subcapsular petechiae
histologic feature of TMA
occluded glomerulal capillaries by platelets and fibrin
thickened capillary walls due to swelling and subendothelial deposits
chronic TMA is confined to patients with
atypical HUS and TTP
gross features of chronic TMA
various degrees of scarring
histologic features of chronic TMA
tam tracks
onion skinning
hypoperfusion
ischemic atrophy
unilateral renal artery stenosis can lead to
hypertension
bilateral renal artery disease leads to
chronic ischemia with renal insufficiency sometimes in the absence of HTN
atheroembolic renal disease can be recognized by
rhomboid clefts or cholesterol crystals in the lumens and walls of arcuate and intralobular arteries
most common clincal and functional abnormalities in sickle cell nephropathy
hematuria
hyposthenuria
major source of emobli in renal artery infarct
mural thrombosis in the left atrium and ventricle as a result of MI
gross features of renal infarct
multiple or bilateral base is along the surface of the kidNey, apex at area of occlusion wedge shaped well delineated white infarct heal with a scar
ischemic coagulative necrosis in renal infarcts present with
intense eosinophilic staining
autosommal recessive renal cystic dses
childhood polycystic
familial juvenile nephrophthisis
autosommal dominant renal cystic dses
adult polycystic kidney dse
adult onset medullary cystic dse
familial juvenile nephrophthisis and adult onset cystic dse present as
corticomedullary cysts
shrunken kidneys
complications of adult polycystic renal disease
hematuria flank pain urinary tract infection renal stones hypertension
complication of childhood polycystic kidney dse
hepatic fibrosis
typical outcome of childhood polycystic disease
variable
death in infancy or childhood
benign renal cystic dses
medullary sponge disease
simple cysts
unrelieved obstruction leads to
hydronephrosis or obstructive uropathy
common causes of urinary tract obstruction
urolithiasis congenital strictures prostate enlargement tumors sloughed clots, papillae pregnancy neurogenic
gross feature of urinary tract obstruction
dilatation of renal pelvis extending to calyxes
loss or atrophy of renal tissue
thinning of parenchma
urolithiasis peak age of onset
20-30 usually in men
causes of urolithiasis
calcium oxalate or phosphate
magnesium ammonium phosphate
uric acid
infections due to proteus present as
staghorn calculi of magnesium phosphate stones
benign renal cell neoplasms
papillary adenoma
angiomyolipoma
oncocytoma
disease associated with angiomyolipoma
tuberous sclerosis
loss of function mutation in tuberous sclerosis
TSC1 or TSC2
large neoplastic cells with vesicular nuclei
abundant eosinophilic granular cytoplasm
oncocytoma
most common primary tumor of the kidney
3% of visceral cancers
adenocarcinoma of the kidney
renal cancer is mostly sporadic but autosomal dominant forms occur in young individuals
von Hippel-lindau syndrome
hereditary (familial) clear cell carcinoma
hereditary papillary carcinoma
genetic features of clear cell RCC
3p-/VHL mutations, inactivations,losses
papillary RCC genetic features
7+/ cnet mutations, 17+, other losses or gains
chromophobe RCC genetic features
…10-,13-,17-,21-
collecting duct carcinoma genetic features
deletion 1q32, 1-32.2,1-,14-,15-,22-
epidemiology of RCC
male 6th-7th decade of life tobacco obesity in women htn unoppesed estrogen therapy exposure to asbestos, petroleum pdTs, heavy metals
most common classification of RCC
clear cell variant
mutation in RCC
3p25
loss of sequences in the short arm of chromosome 3
gross features of RCC clear cell variant
golden yellow mass with irregular borders distorting the outline of the kidney
histologic features of RCC clear cell variant
acinar or tubular growth pattern with clear cell cytoplasm
most common type of RCC in patients who develop dialysis associated cystic disease
papillary tumor RCC
papillary tumor variant RCC arises form the
DCT
papillary tumor variant RCC is not associated with ch 3p deletions but in
chromosome 7
gross features of papillary tumor RCC
multifocal
bilateral
hemorrhagic
brownish discoloration
histologic features of papillary RCC
papillary
cuboidal or low columnar neoplastic cells
abundant histiocytes within the papillary core
psamomma bodies
stroma scanty but highly vascularized
most reliable symptom of RCC
hematuria
other features of RCC
costovertebral pain
palpable mass
tendency to metastasize
poor prognosis of RCC
when the tumor encroaches the renal pelvis at the insertion or entrance of the renal vein or artery
transitional CA usually arise from
renal pelvis-hilum
tumor stage at the renal vein, vena cava or regional lymph nodes
stage 3
tumor beyod gerota’s fascia
stage 4
