Kidney Pathology Flashcards
[diagnosis: glomerular response to injury]
acute, proliferation of mesangium/endothelial cells (hypercellularity), crescent formation
PSGN
[diagnosis: glomerular response to injury]
deposition of electron-dense material, synthesis of protein component of GBM, additional layers of BM matrices,
membranous nephropathy
[diagnosis: glomerular response to injury]
deposition of homogenous eosinophilic material, deposition of collagen
FSGS
[diagnosis]
hematuria, azotemia, edema, hypertension, variable proteinuria
nephritic syndrome
[diagnosis]
acute nephritis, proteinuria, acute renal failure
RPGN
[diagnosis]
> 3.5g/day proteinuria, hypoalbuminemia, hyperlipidemia, lipiduria
nephrotic syndrome
[diagnosis]
azotemia, uremia progressing for months to years
chronic renal disease
[diagnosis]
Glomerular hematuria and/or subnephrotic proteinuria
isolated urinary abnormalities
[diagnosis]
diffuse global hypercellularity, swelling of endothelial cells, obliterates capillary lumina, tubulointerstitial edema and inflammation, with RBC casts
EM: subepithelial humps on GBM
IF: granular deposits of IgG, C3, and Ig within the wall and mesangium
PSAGN
[diagnosis]
prototype renal disease of type III hypersensitivity reactions
PSGN
laboratory finding elevated in PSGN after pyoderma
Anti DNAse B
[diagnosis]
progressive loss of renal function characterized by nephritic syndrome with severe oliguria
proliferation of parietal epithelial cells admixed with leukocytes infiltrating the glomerulus (“crescents”)
EM: rupture in GBM
IF: linear IgG and C3 deposits along GBM
RPGN TYPE I
AntiGBM Disease
Goodpasture Syndrome
[diagnosis]
progressive loss of renal function characterized by nephritic syndrome with severe oliguria
proliferation of parietal epithelial cells admixed with leukocytes infiltrating the glomerulus (“crescents”)
EM: lumpy bumpy appearance of GBM
IF: granular IgG and C3 deposits in GBM
RPGN type II
PSAGN, Lupus Nephritis, HSP, Buerger disease
[diagnosis]
progressive loss of renal function characterized by nephritic syndrome with severe oliguria
proliferation of parietal epithelial cells admixed with leukocytes infiltrating the glomerulus (“crescents”)
EM: no detectable deposits
IF: negative IgG and C3 deposits along GBM
RPGN type III
ANCA vasculitides
[diagnosis]
20 y/o male, active smoker with hemoptysis AND renal failure
necrotizing hemorrhagic interstitial pneumonitis + RPGN
RPGN Type I
Goodpasture Syndrome
20 y/o male, active smoker with hemoptysis AND renal failure
necrotizing hemorrhagic interstitial pneumonitis + RPGN LIMITED to kidneyonly
RPGN Type I
Anti-GBM disease
[diagnosis]
children, no azotemia, on recent prophylactic immunization, with nephrotic syndrome
LM: no changes
EM: uniform and diffuse effacement of foot processes of the podocyte
IF: no changes
Minimal Change Disease
[diagnosis]
adult, with SLE and EBV infection, taking NSAIDs
LM: diffuse thickening of capillary wall
EM: subepithelial deposits along GBM (spike and dome appearance); effacement of foot processes
IF: granular deposit of immunoglobulin and complement along the GBM
Membranous Glomerulonephropathy
[diagnosis]
adult, with HIV on heroin
LM: deposition of hyalin masses, increased mesangial matrix in nonaffected segments
EM: effaced foot process
IF: non-specific trapping of IgM and C3 in areas of hyalinosis
FSGS
[diagnosis]
patient with schistosomiasis
LM: thickened split GBM (tram track)
EM: subENDOthelial electron-dense deposits
IF: irregular, granular C3 deposit WITH IgG and C1q and C4
MPGN Type I
Both classical and alternative pathways are active
[diagnosis]
patient with Factor H mutation, with ESRD
LM: thickened split GBM (tram track)
EM: lamina densa and glomerular capillary transformed into irregular, ribbon-like, dense structure
IF: irregular, chunky, segmental linear foci of C3 deposits in GBM and mesangium WITHOUT IgG and complement
MPGN Type II
Alternative pathway is active
Also called Dense Deposit Disease
[diagnosis]
Young adult with previous GIT infection
LM: mesangial widening and endocapillary proliferation
EM: mesangial electron dense deposits
IF: mesangial deposition of IgA, often with C3 and properdin
localized to kidneys
IgA nephropathy (Berger Disease)
most common type of GN worldwide
IgA nephropathy
[diagnosis]
6 year old child with purpuric lesion, abdominal pain, intestinal bleeding, arthralgial with renal abnormalities
LM: mesangial widening and endocapillary proliferation
EM: mesangial electron dense deposits
IF: mesangial deposition of IgA, often with C3 and properdin
systemic deposition of IgA
HSP
[diagnosis]
male with lens dislocation, posterior cataract, corneal dystrophy, deaf, hematuria
LM: glomerulosclerosis, tubular atrophy
EM: thin GBM, basket-weave appearnce of GBM
Alport syndrome
[diagnosis]
X-linked Dominant, defective Type IV collagen with CKD
Alport syndrome
[diagnosis]
symmetrically contracted kidneys, thin cortex, increase in peripelvic fat,
Microscopically: hyalinosis and sclerosis, arterioloscleorsis, tubular atrophy, mononuclear infiltrates and fibrosis of interstitium
chronic GN
[type of ATN]
patchy, short; straight segments of proximal tubule and ascending loop of henle are affected
present cast
ischemic ATN
[type of ATN]
extensive, long; affected are PCT and ascending loop of henle
present cast
toxic ATN
[type of tubulointerstitial nephritis]
(+) interstitial edema
(-) fibrosis
(-) atrophy
neutrophils and eosinophils dominate
Acute TIN
[type of tubulointerstitial nephritis]
(-) interstitial edema
(+) fibrosis
(+) atrophy
mononuclears (lymphocyte predominance)
Chronic TIN
most common cause of AKI
Acute tubular necrosis
second most common cause of AKI
tubulointerstitial nephritis caused by drugs/toxins
most common route of UTI in females
ascending infection
most common agents that cause UTI via ascending infection
E.coli
Proteus
Enterobacter
[diagnosis: form of pyelonephritis]
female with uncontrolled DM
fever, CVA tenderness, dysuria
pyuria, bacteriuria, WBC casts
Acute Pyelonephritis
[diagnosis: form of pyelonephritis]
8 year old male with vesicoureteral obstruction
blunting, flattening, loss of papilla, no abscess
thyroidization, tubular atrophy, and vascular sclerosis in scarred areas
chronic pyelonephritis
[diagnosis: vascular disorders]
patient with essential hypertension, leathery granular kidneys, with hyaline arteriolosclerosis, not in uremia
nephrosclerosis
[diagnosis: vascular disorders]
patient with malignant hypertension, petechial hemorrhages on surface, hyperplastic arteriosclerosis (onion-skinning)
patient became uremic
malignant nephrosclerosis
[diagnosis: vascular disorders]
hyaline arteriolosclerosis; hyaline deposition
essential HPN
[diagnosis: vascular disorders]
hyperplastic arteriolosclerosis
fibrinoid necrosis
malignant hypertension
onion-skinning
[diagnosis: cystic diseases]
ADPKD are commonly seen among ___ (adults/children)
adults
[diagnosis: cystic diseases]
ARPKD are commonly seen among ___ (adults/children)
children
[diagnosis: cystic diseases]
patient with renal failure, liver cyst, intracranial berry aneurysm, mitral valve prolapse
ADPKD
most common cause of death is Coronary or HHD
[diagnosis: cystic diseases]
patient with renal failure with periportal fibrosis
ARPKD
[diagnosis: cystic diseases]
PKD1 and PKD2 mutation
ADPKD
[diagnosis: cystic diseases]
PKHD 1 mutation
ARPKD
[identify the type of renal stone]
radiopaque, octahedron shape
Acidic urine pH
calcium oxalate
[identify the type of renal stone]
radiopaque, coffin-lid shape
basic urine pH
struvite
[identify the type of renal stone]
radiolucent, rhombic shape
acidic urine pH
uric acid
[identify the type of renal stone]
radiopaque but difficult to visualize than Ca stones, hexagonal
acidic urine pH
cystine stone
[identify the type of renal stone]
proteus infection, staghorn calculi
basic pH
struvite stones
[diagnosis]
hematuria, flank pain, palpable mass
from proximal tubule cells
yellowish mass with areas of necrosis
histo: rounded or polygonal cells with abundant clear or granular cytoplasm which contains glycogen or lipids
clear cell
[diagnosis]
hematuria, flank pain, palpable mass
renal CA associated with von hippel lindau syndrome
clear cell
[diagnosis]
hematuria, flank pain, palpable mass
from distal tubule cell, hemorrhagic with cystic mass
histo: psammoma bodies present, cuboidal or low columnar cells in papillary formations
papillary
[diagnosis]
hematuria, flank pain, palpable mass
from intercalated cells of Cajal (collecting duct)
mahogany brown, relatively homogenous, well-encapsulated with central scarring
histo: pale eosinophilic cells with perinuclear halo, arranged in solid sheets with a concentration of the largest cell around blood vessels
chromophobe
renal cell CA ha a tendency to invade what vein
renal vein
