Exam 1 Path/Clinical Flashcards
Azotemia
increased serum BUN/creatinine
decreased GFR
Cause of prerenal azotemia
kidney hyoperfusion
Nephritic sx
<3.5 protein loss per day azotemia HTN hematuria inflammatory process
Nephrotic sx
> 3.5 protein loss per day
hypoalbuminemia
hyperlipidemia
Cause of hyalinosis
accumulation of eosinophilic material
Acute proliferative GN characteristics
post-strep GN, 1-4wks after
6-10y/o
immune complex deposition
glomerular proliferation
Acute proliferative GN histo
hypercellularity
red cell casts
mesangial/GBM deposition of IgG/IgM/C3
Sx of acute proliferative GN
young child post sore throat
red cell casts in urine
periorbital edema
decreased serum C3
Rapidly progressive GN characteristics
crescentic GN
loss of renal fxn
epithelial proliferation
oliguria/nephritic syndrome
Types of rapidly progressive GN
Anti-GBM (Goodpastures)
immune complex deposition (HSP)
Pauci-immune (c-ANCA)
Fluorescence of RPGN types
anti-GBM- linear
immune complex- granular
pauci-immune- no deposition
Clinical sx of rapidly progressive GN
hematuria
HTN/edema
anti-GBM/ANA/ANCA abs depending on type
Membranous nephropathy characteristics
irregular immune complex deposition
granular on IF
nephrotic syndrome in adult whites
assc with SLE/tumors/infections
Clinical sx of membranous nephropathy
nephrotic syndrome
hematuria
mild HTN
sclerosis of glomeruli
Minimal change disease characteristics
ages 2-6
follow infection or vaccine
nephrotic syndrome in children
response to corticosteriods
Minimal change disease sx
massive proteinuria
good renal fxn
assc with Hodgkin lymphoma in adults
Focal segmental glomerulosclerosis characteristics
nephrotic syndrome
ass with Sickle Cell/HIV/heroin use/blacks
Focal segmental glomerulosclerosis histo
lipid droplets/foam cells hyalinosis of afferent arterioles retraction/collapse of glomeruli effacement of foot processes (flattening) IgM/C3 in mesangium
Membranoproliferative GN characteristics
nephrotic/nephritic combo
hypercellular glomeruli
crescents
tram track appearance with silver stain
Type 1 MPGN
subendothelial deposits
granular C3 deposition, some IgG
Type II MPGN
ribbon like, irregular GBM
granular or linear
C3 in mesangium in circular ring
no IgG/Cl4/C4
IgA nephropathy characteristics
Berger disease
IgA deposition in mesangium
hematuria
nephritic/sometimes nephrotic
Microscopy of IgA nephropathy
mesnagial IgA deposition
C3/properdin
Henoch-Schonlein purpura characteristics
purpuric skin lesions on arm/legs nonmigratory arthralgias hematuria nephritic/nephrotic syndromes 3-8y/o follows URT infection
Morphology of HSP
crescentic glomerulonehpritis
mesangial proliferation
deposition of IgA in mesangial regions
Alport syndrome characteristics
hematuria/red cell casts nerve deafness eye disorders X-linked 5-20y/o
Alport syndrome morphology
GBM thinning
splitting of lamina dense (basket weave appearance)
glomerulosclerosis
Chronic glomerulonephritis characteristics
crescentic glomerulonephritis
contraction of kidneys
thin cortex
atrophy of tubules
Micro and macroabluminuria levels
micro: 30-300mg/day
macro: >300mg/day
Urinalysis measurement
only albumin
Nephrotic syndrome in children
minimal change disease
Nephrotic syndrome with adults
membranous and focal sclerosis
Complications of nephrotic syndrome
hyperlipidemia
hypercoagulability
Tubular proteinuria protein loss
no albumin loss
500-2000mg/day
Orthostatic proteinuria protein loss
daytime urine has higher proteinuria
Overflow proteinuria protein loss
light chains/small MW proteins lost
multiple myeloma assc
False (+) for hematuria
foods/drugs
myoglobing-rhabdomyolysis (no RBC’s)
What are red blood cell casts?
Tamm Horsfall protein + RBC’s in tubules
Demographic for minimal change disease
children
Demographic for focal segmental GN
black
HIV
heroin users
Demographic for membranous nephropathy
caucasian adults
Demographic for IgA nephropathy
Asian
Hispanics
American Indian
Microscopy of minimal change disease
fusion of foot processes
Microscopy of focal segmental GN
focal/segmental damage
Microscopy of membranous nephropathy
subepithelial immune deposits (PLA2R)
thick basement membrane
Microscopy of IgA nephropathy
mesangial IgA deposition
Nephrotic syndromes
minimal change disease
focal segmental GN
membranous nephropathy
Postinfection GN characteristics
2-3wks post infection
nephritic
low complement
subepithelial humps
Membranoproliferative GN
assc with Hep C
cryoglobulinemia
nephritic syndrome/sometimes nephrotic
Types of cryoglobulinemia
I-monoclonal IgM, multiple myeloma/Waldenstrom assc
II-monoclonal IgM against IgG
III-polyclonal IgM against IgG, Hep C/rheumatoid factor assc
Glomerulonephritis diseases with low serum complement
post infection
membranoproliferative
cryoglobulinemia
lupus nephritis
Membranoproliferative GN microscopy
splitting of thick membranes
tram tracking
cryoglobulin precipitates in capillaries
subendothelial immune complex deposition
Hyperacute transplant rejection cause
preformed Abs react with allo-Ags
thrombosis/necrosis results
Membranoproliferative GN type 1
C3 and IgG/IgM
classic C pathway
rail track appearance
Membranoproliferative GN type 2
C3 nephritic factor, C3 convertase stabilized
alternative C pathway
ribbon appearance
Focal segmental GN asscs
HIV
heroin use
Sickle cell disease
Hispanics/blacks
Membranous nephropathy assc
white adult male Hep B/C tumors SLE drugs (NSAIDS/penicillamine)
Diabetes mellitus characteristics on kidneys
nonenzymatic glycosylation
results in hyaline arteriolosclerosis
Kimmelstiel-Wilson nodules
Systemic amyloidosis characteristics on kidneys
amyloid deposits in mesangium
nephrotic syndrome
Congo red/apple green birefringence
Nephrotic syndrome groupings
FSGS/MCD- foot process effacement
MN/MPGN-deposits of immune complexes
DM/amyloidosis-nodular glomerulosclerosis
Ischemic acute kidney injury sign
hyaline/granular casts
from Tamm Horsfall protein
Toxic acute kidney injury causes
HgCl-acidophilic inclusions
CCl4-neutral lipids in cells
Ethylene glycol-vacuolar degeneration/calcium oxalate crystals
Acute pyelonephritis immune cells present
neutrophils
Chronic pyelonephritis morphology
thyroidization-flat epithelium/dilated tubules
fibrosis
Analgesic nephropathy clinical picture
women with muscle pain
hypochondriac
Urate nephropathy types
uric acid crystals/lymphoma
monosodium urate crystals/Tophus
uric acid stones/gout
Types of urolithiasis
calcium oxalate/phosphate, most common
Mg/ammonium/phosphate, bacterial/staghorn stone
uric acid, radiolucent
cystine, congenital defect
AD polycystic kidney disease
bilateral enlarged kidneys
cysts filled with serous/red-brown fluid
from tubules
AR polycystic kidney disease
PKHD1/2 gene mutation childhood onset smooth external surface of kidney spongelike appearance with small cysts portal fibrosis/liver cysts
Medullary sponge kidney
dilation of medullary collecting ducts
assc with Marfans/Carolis/Ehlers-Danlos
sponge like appearance of medulla
Renal papillary adenoma
branching/papillomatous structure
metastasizes over 3cm
Angiomyolipoma
hamartoma
assc with tuberous slcerosis
spontaneous hemorrhage assc
Oncocytoma
tan/mahogany brown color
well encapsulated
lg eosinophilic cells
Renal cell carcinoma
yellow color
60-70’s
tobacco increases risk
from tubular epithelium
Clear cell carcinoma
most common renal cell carcinoma
orange/yellow color
upper pole of kidney
chromosome 3p deletion
Asscs with clear cell carcinoma
von Hippel-Lindau
tuberous sclerosis
Papillary carcinoma
fibrous capsule
foamy macrophages/intracellular hemosiderin
Genetics of papillary carcinoma
sporadic: trisomy 7,16.17, loss of Y
familial: trisomy 7
Chromophobe renal carcinoma
tan brown/well circumscribed
compact architecture of nests
halo around nuclei
(+) Hale’s colloidal iron stain
Collecting duct carcinoma
Bellini duct carcinoma
infiltrative borders
hobnail cell lined
mucin producing/desmoplastic response
Acute transplant rejection
5-7 days after transplant
HS type IV
immunosuppression helps
lymphocytes predominant cell type
Benign nehproslcerosis
caused by HTN
hyaline arteriosclerosis
assc with diabetes and fibromuscular dysplasia
Malignant nephrosclerosis
from malignant HTN
uremia causes death
fibrinoid necrosis/hyperplastic arteriosclerosis
angiotensin II released, perpetuates damage
Renal artery stenosis
number 1 cause-atheromatous plaque
number 2-FMD, women 20-40y/o
Factors with thrombotic microangiopathy
endothelial injury-vasoconstriction
platelet aggregation-von Willebrand factor/ADAMTS-13
Childhood hemolytic uremic syndrome
follows EHEC infection
shigella like toxin
assc with petting zoos/undercooked meats
Verocytotoxin causes platelet aggregation
Adult (atypical) hemolytic uremic syndrome causes
SLE pregnancy malignant HTN immunosuppressants factor H complement defect
Thrombotic thrombocytopenic purpura
hemolytic anemia
purpura
neuro sx
caused by defect of ADAMTS-13 (thins blood)
ANCA (+) disease
Wegener’s granulomatosis
microscopic polyangitis
Churg-Strauss syndrome
Wegener’s granulomatosis
chronic sinusitis
ANCA (+)
noncaseating granulomas
nephritic syndrome
Microscopic polyangitis vs Wegener’s granulomatosis
similar to Wegener’s but no granulomas
Isolated pauci-immune GN vs Wegener’s granulomatosis
Wegener’s but limited to the kidney (no lung involvement)
Churg-Strauss syndrome
allergic rhinitis worsening asthma rash with palpable purpura peripheral neuropathy nephritic syndrome ANCA (+) eosinophilia with small vessel vasculitis
Goodpasture’s disease
anti-GBM against lungs and kidneys
nephritic syndrome
crescentic, necrotizing GN
linear deposition of IgG on IF
Lupus nephritis
young women with SLE
can mimic any glomerular disease
“full house” on IF
SLE sx
photosensitive rash
Raynaud’s
alopecia
anti-dsDNA and ANA (+)
Diabetic nephropathy
Kimmelstiel-Wilson nodules
nonenzymatic glycosylation
Amyloidosis on kidneys
primary-light chains assc with multiple myeloma
secondary-amyloid
Congo red/apple green birefringence
Sickle cell disease on kidneys
hematuria/proteinuira from sickled cells
decreased renal conc mechanism
Diffuse cortical necrosis causes
OB emergency
septic shock
extensive surgery
Henoch-Schonlein purpura
small vessel vasculitis
palpable purpura with IgA deposits on bx
children/young adults following URT infection
HIV assc nephropathy
increased in blacks
FSGN
collapsing glomeruli
Minimal change disease findings
foot process effacement
Membranous GN findings
granular IF
subepithelial deposits
Focal segmental GN findings
no deposits on EM
segmental GS
IgA nephropathy findings
mesangial proliferation
IgA deposits in mesangium
Post strep GN/acute proliferative GN findings
garland on IF
subepithelial deposits
ANCA diseases findings
crescentic, necrotizing GN
no deposits/IF
Goodpasture’s findings
crescentic, necrotizing GN
linear IF
no deposits
Membranoproliferative GN findings
granular IF
subendothelial/mesangium deposits
tram track appearance (membrane splitting)
Lupus findings
“full house” on IF
any histo of other diseases
Diabetes mellitus findings
nodular GS
thick basement membrane
Amyloidosis findings
nodular GS
Congo red (+)
fibrils
HIV assc nephropathy findings
collapsing FSGN
reticular inclusion bodies
