OS 214 Renal Pathology Pictures Flashcards
Identify the pointed structure (from Rosai & Ackerman)
Foot processes (epithelial aspect of BM). Electron micrograph of normal glomerulus. EN (endothelial cell); EP (epithelial cell); ME (mesangium).
Identify (from Rosai & Ackerman).
Minimal change disease (minimal abnormality in LM). Glomerulus normocellular, BM normal thickness. Most common cause of nephrotic syndrome in children. Characterized by diffuse effacement of foot processes in EM.
Identify (from Rosai & Ackerman).
Minimal Change Disease in EM. Note effacement of foot processes.
Identify (from trans)
FSGS under LM. With segmental sclerosis (pointed), and obliteration of glomerular capillaries.
Identify (from trans).
FSGS under LM with hyalinosis (pointed).
Identify (from Rosai & Ackerman)
FSGS under IF. (+) segmental deposition of IgM.
To differentiate from MCD:
Under LM, FSGS is already present. MCD looks normal.
Under IF: MCD is usually negative for Igs and C3.
Identify (from trans).
Membranous glomerulopathy (LM). Note normal to diffuse thickening of capillary wall. (+) foam cells in interstitium.
Identify (from Rosai & Ackerman)
MGN. Silver preparation showing “spike” formation along thickened BM.
Identify (be specific) (from Rosai & Ackerman).
MGN Stage I (EM). BM normal thickness. (+) subendothelial deposits (arrows). Epithelial foot processes obliterated.
Identify (be specific) (from Rosai & Ackerman).
MGN Stage II. Subepithelial deposits at regular interval, separated by projections of BM.
Identify (be specific) (from Rosai & Ackerman).
MGN Stage III. BM markedly thickened; deposits appear to be surrounded by newly formed BM (arrows).
Identify (be specific) (from Rosai & Ackerman).
MGN Stage IV. BM markedly irregular; deposits lysed, leaving large electron-lucent areas;
“moth-eaten appearance”
Identify (from Rosai & Ackerman).
MGN. (+) Peripheral GRANULAR deposits of IgG +/- C3.
Identify (from trans).
Membranoproliferative GN - (+) mesangial cell proliferation, BM thickening, & leukocyte infiltration (top image); MPGN under IF (bottom image).
Identify A & B (from trans).
A - MPGN Type I.
B - MPGN Type II/”Dense Deposit Disease”
Identify (from Rubin’s, not Robbin’s haha)
FSGS (PAS stain). Note perihilar areas of segmental sclerosis and adjacent adhesions to Bowman’s capsule.
Identify (from Rubin’s).
FSGS in HIV nephropathy (silver stain).
Identify (from Rubin’s; don’t mind the number haha)
Membranous glomerulonephritis. Glomerulus slightly enlarged and shows diffuse thickening of capillary walls. No hypercellularity.
Identify (from Rubin’s)
Membranous glomerulopathy, Stage II (EM). Deposits of electron-dense material (arrows), with intervening projections of BM material.
Identify (from Rubin’s).
Membranous glomerulopathy (IF). (+) granular deposits of IgG outlining capillary loops.
Identify (from Rubin’s).
Diabetic glomerulosclerosis (PAS stain). There is increase in mesangial matrix, forming several nodular lesions. Some capillary BM thickened, dilation of glomerular capillaries evident.
Identify (from Rubin’s).
Amyloid nephropathy.
Identify (from Rubin’s).
Amyloid nephropathy (congo red stain). Amyloid deposits show characteristic APPLE-GREEN BIREFRINGENCE.
Identify (from Rubin’s).
Alport Syndrome (hereditary nephritis). Note “BASKET WEAVE” appearance - lamina densa of glomerular BM is laminated (arrows) rather than forming a single dense band.
Due to mutations in genes that encode Type IV collagen (alpha 3,4,5 chains).
Identify (from Rubin’s).
Acute poststreptococcal glomerulonephritis (Masson-Trichome stain) with numerous neutrophils.
Identify (from Rubin’s).
Acute postinfectious glomerulonephritis (EM). With numerous subepithelial “HUMPS” (arrows).
Identify (from Rubin’s).
MPGN Type I. Glomerular lobulation accentuated; increased cells and matrix in the mesangium and thickening of capillary walls are noted.
Identify (from Rubin’s).
MPGN Type II. Capillary wall thickening, hypercellularity, and a small crescent are evident.
Identify (from Rubin’s).
MPGN Type II / “Dense deposit disease” with RIBBON-like appearance due to linear deposition of PAS-positive material along BM.
Identify (from Rubin’s).
MPGN Type I (IF). Granular to band-like staining for C3 in capillary walls and mesangium.
Identify (from Rubin’s).
MPGN Type II (IF). Bands of capillary wall staining and coarsely granular mesangial staining for C3.
Identify (from Rubin’s).
Proliferative lupus glomerulonephritis (LM). Hypercellularity and thickening of capillary walls present.
Identify (from trans) + type of RPGN.
SLE (IF). Type II RPGN. - characteristic “FULL HOUSE” configuration (for higher learning lang haha, since can’t be differentiated without the proper marker testing)
Identify (from Rubin’s).
IgA nephropathy (Berger’s disease) (IF). Deposits of IgA in mesangial areas.
Identify (from Rubin’s).
IgA nephropathy (PAS stain). Segmental mesangial HYPERcellularity and matrix expansion caused by mesangial immune deposits.
Identify (from Rubin’s).
IgA nephropathy (EM). With prominent dense deposits in mesangial matrix (arrow).
Identify + type of RPGN (from trans).
SLE. Type II RPGN (immune-complex). Fingerprinting and curvilinear pattern.
Identify + type of RPGN (from Rubin’s).
Anti-GBM glomerulonephritis. LINEAR deposits. Type I RPGN. Associated with pulmonary hemorrhage.
Identify + type of RPGN (from Rubin’s).
Anti-GBM, type I RPGN. Bowman space filled with cellular crescent (Masson-trichome stain).
Identify + Type of RPGN (from Rubin’s).
ANCA glomerulonephritis. RPGN Type III (pauci-immune). Segmented fibrinoid necrosis illustrated.
Identify (from trans).
Chronic GN. With sclerosis, fibrosis, atrophy, and thickening of blood vessels.
Poststrep GN, RPGN, MGN, MPGN, FSGS, IgA can all lead to Chronic GN.
Identify (from Lab Trans).
Acute GN. Shows enlarged hypercellular glomeruli due to:
- infiltration of neutrophils and monocytes
- proliferation of endothelial and mesangial cells
- crescent formation (proliferation of the parietal epithelium)
Identify (from Lab Trans).
Acute Tubular Necrosis.
-evidenced by
the disrupted cell
architecture, granular,
eosinophilic cytoplasm and
desquamation of the
tubular epithelium
-in urinalysis: with MUDDY BROWN CASTS
Identify (from Rosai & Ackerman).
Polyarteritis nodosa. Fibrinoid necrosis involving two medium-sized arteries.
Identify (from trans).
Thin Basement Membrane Disease. Shows thinning of GBM (arrows) and effacement (minimal change disease).
Identify (from trans).
Diabetic glomerulosclerosis.
Identify A & B (from trans).
(A) Fibrillary GN showing slightly curved fibrils
(12-16mm in diameter) relatively thinner than
(B) Immunactoid
GN presenting with thick fibrils (48-55mm in diameter),
appearing as microtubules with electron lucent center
Identify (from trans).
Essential Mixed Cryoglobulinemia under EM
showing (left) deposits within phagolysosomes of mononuclear
phagocytes and (right) deposits with microtubular profiles.
Identify (from trans).
Plasma cell dyscrasias
showing (A) light
chain myeloma casts with fractures, polychromasia, leukocytic
reaction, and tubule cell damage [H&E]; (B) light chain deposition
glomerulus with increased lobulation and hypercellularity [H&E];
(C) IF showing bright linear stains of lambda light chains [TBM, no
stain for kappa]; (D) EM showing fine granular deposits within
GBM
Identify (be specific) (from Rubin’s).
Ischemic acute tubular necrosis. Note lack of interstitial inflammation and presence of some regenerative-appearing epithelial cells.
Identify (be specific) (from Rubin’s).
Toxic acute tubular necrosis. Interstitial inflammation minimal; there is widespread necrosis of proximal tubular epithelial cells, with sparing of distal and collecting tubules.
Identify (from Rubin’s).
ACUTE pyelonephritis. There is extensive infiltrate of neutrophils present in collecting tubules and interstitial tissue. “Parang nilalanggam”.
Identify (be specific) (From Rubin’s).
CHRONIC pyelonephritis. With many tubules containing eosinophilic hyaline casts resembling colloid of of thyroid follicles (THYROIDIZATION). The interstitium is scarred and contains a chronic inflammatory infiltrate.
Identify (from Lab Trans).
Xanthogranulomatous Pyelonephritis. Characterized by accumulation of FOAMY MACROPHAGES mixed with plasma cells, lymphocytes, leukocytes, and a few giant cells.
Usually related to PROTEUS infection and/or obstruction.
Identify (from Lab Trans).
Renal Infarction.
Usually of the
coagulative or “white”
type, due to lack of
collateral blood supply
• Wedge-shaped, pale
areas with apex at the
medulla, and showing
coagulative necrosis
Identify (from Lab Trans).
Benign Nephrosclerosis.
• Thickening and hyalinization
of arteriolar walls and small
arteries (hyaline
arteriolosclerosis)
• May be accompanied by
medial and intimal
thickening of the interlobar
and arcuate arteries
(fibroelastic hyperplasia)
• Vascular narrowing may
cause patchy ischemia with
tubular atrophy, instertitial
fibrosis, and glomerular
alterations
Identify (from Lab Trans).
Renal Cell Carcinoma (Conventional Type)
• Solid, trabecular or tubular
proliferation of large, round
to polygonal cells. Cytoplasm
varies form clear with sharply
outlines boundaries
(vegetable cells), to deeply
granular
• May be occasional central,
rounded luminal spaces with
lightly eosinophilic serous
fluid
• Contains regular network of
small, thin-walled blood
vessels
• Nuclei are usually
centrally located; and
the level of its atypia is
used for histologic
grading
Identify (from Lab Trans).
Infiltrating Transitional Cell Carcinoma.
• Arises from urothelium of
renal pelvis , and is
histologically similar to
bladder counterparts
• Infiltrating type has
cohesive nests of cells
with moderate to
abundant amphophilic
cytoplasm
• Palisading of nuclei may
be seen at edges of large
nests
• Cells have large,
hyperchromatic,
pleomorphic nuclei with
irregular contours and
angular profiles. Nucleoli
are variable
Identify (from Lab Trans).
Angiomyolipoma.
• Composed of variable
mixture of mature fat,
thick-walled poorly
organized blood vessels,
and smooth muscles that
appear to radiate from
the blood vessels walls
• Sharp demarcation from
surrounding kidney, with
occasional entrapped
renal tubules at its
periphery
Identify (from Lab Trans).
Renal Tuberculosis.
• Presence of chronic
granulomatous
inflammation with
caseation necrosis and
Langhan type giant cells
in the renal parenchyma
Identify (from Lab Trans).
Uteritis.
• Inflammation of the
ureter, usually not
associated with infection
and of little consequence
• Mucous may have fine
cysts (ureteritis cystica)
or germinal centers
(ureteritis follicularis)
Identify (from Rubin’s).
Staghorn calculi.
Identify (from Rubin’s).
Hydronephrosis.
Identify (from Rubin’s).
Wilm’s tumor.
Identify (from Rubin’s).
Clear cell renal cell carcinoma.
Yellow areas correspond to lipid-containing cells.
Identify (from Rubin’s).
Clear cell renal cell carcinoma. Island of neoplastic cells with abundant clear cytoplasm.
Identify (from Rubin’s).
Papillary renal cell carcinoma. (+) Papillary fronds covered by neoplastic cells.
Identify (from Rubin’s).
Chromophobe renal cell carcinoma.
-pale acidophilic granular cells with prominent cell borders.
Identify (from Rubin’s).
Acute cystitis.
Identify (from Rubin’s).
Acute cystitis. With PMN leukocytes infiltrate the mucosa.
Identify (from Rubin’s).
Chronic cystitis.
-nonspecific inflammatory infiltrate
composed of lymphocytes and plasma cells is present in the edematous
lamina propria.
Identify (from Rubin’s).
Uteritis cystica.
Identify (from Rubin’s).
Urothelial cell carcinoma in situ.
-mucosa
shows nuclear pleomorphism and lack of polarity from the basal layer
to the surface, without evidence of maturation
Identify (from Rubin’s).
Urothelial carcinoma of the bladder.
-exophytic tumor situated above the bladder neck
Identify (from Rubin’s).
Low grade papillary urothelial carcinoma.
-consists of exophytic
papillae that have a central connective tissue core and are lined by slightly disorganized transitional epithelium.
Identify (from Rubin’s).
High grade papillary urothelial carcinoma.
C. High-grade
papillary urothelial carcinoma shows prominent architectural disorganization of the epithelium, which contains cells with
pleomorphic hyperchromatic nuclei.
D. Invasive high-grade papillary urothelial carcinoma consists of irregular nests of
hyperchromatic cells invading into the muscularis.
Identify (from Patho Plenary trans).
Wilm’s Tumor.
-Pale staining
stroma (light pink) alternating with darkly staining undifferentiated
blastemal component (dark violet. Not leukocytes). Within the
blastema, epithelial differentiation in the form of irregular ribbons
and tubules is seen (encircled)
Identify (from Patho Plenary Trans).
Wilm’s tumor.
Identify (from Patho Plenary Trans).
Renal cell carcinoma, clear cell type.
This 8 cm carcinoma of the lower pole of
the kidney shows extension beyond the cortical surface, but it does
not infiltrate the perinephric adipose tissue. It is well delineated,
with cystic spaces, lobulated (due to septae), dark yellow in color
(due to lipids). Hemorrhagic necrosis present.
Identify (from Patho Plenary Trans).
Renal cell carcinoma, clear cell type.
Identify (from Gross Lab Trans).
Hydronephrosis.
Identify (from Gross Lab Trans).
Renal tuberculosis. Cheesy friable material (pointed).
Identify (from Gross Lab Trans).
Simple cyst.
1.Perinephric
-came from somewhere else
that seeded into the kidney
(usually hematogenous spread)
2. Nephric
-Came from within the kidney
itself
Identify (from Gross Lab Trans).
Multicystic disease.
types:
1. Autosomal dominant
polycystic kidney disease
(shown in picture)
-adult onset
-with hematuria, mass,
flank pain, htn, renal
failure
2. Autosomal recessive
polycystic kidney disease
-onset: childhood/infancy
-maaga namamatay
Identify (from Gross Lab Trans).
Renal cell carcinoma.
Usual site of metastasis: lungs and bones.
Identify (from Gross Lab Trans).
Urothelial CA/Transitional cell CA
• 2 types of growths:
1. Exophytic/fungating
2. Endophytic
• Bad prognosis since in could travel out to
bladder, ureter etc.
Identify (from Urologic Tumors Trans).
Renal Papillary Adenoma.
Gross and microscopic presentation of RPA. (L) Gross:
discrete, well-circumscribed nodule. (R) Microscope: complex,
branching papillomatous structures with numerous complex
fronds.
• Arise from the renal tubular epithelium
Identify (from Urologic Tumors Trans).
Angiomyolipoma.
Identify (from Urologic Tumors Trans).
Oncocytoma.
-Fairly uniformed cells with sheets or nests appearance
of cells.
Identify (from Urologic Tumors Trans).
Renal papillary carcinoma.
Note the papillae and foamy macrophages in the stalk.
Identify (from Urologic Tumors Trans).
Chromophobe carcinoma.
Note the pale eosinophilic cell with HALO arranged in
solid sheets.
Identify A,B,C & D (from Urologic Tumors Trans).
(A) Carcinoma in situ – full thickness but does not
infiltrate BM; (B) Papillary TCCA; (C & D) TCCA infiltrative
Identify (from Urologic Tumors Trans).
Papillomas.
(L) Cross section of the bladder with upper section
showing a large papillary tumor. Lower section demonstrates
multifocal smaller papillary neoplasm.
(R) Papilloma consisting of
small papillary fronds lined by normal appearing urothelium.
Which is low grade, and high grade papillary urothelial carcinoma (from Urologic Tumors Trans)?
Low grade (L) vs. High grade (R). Low grade PUCA
with an overall orderly appearance, thicker lining than papilloma
and scattered hyperchromatic nuclei and mitotic figure. High
grade PUCA on the other hand shows marked cytologic atypia.
Identify (from Urologic Tumors Trans).
Squamous cell carcinoma (bladder tumor).
(+) KERATIN PEARLS
Identify (from Urologic Tumors Trans).
Adenocarcinoma of the bladder.
Identify (from Radio Lab Trans).
Medullary nephrocalcinosis.
Identify (from Radio Lab Trans).
Nephrolithiasis.
Identify (from Radio Lab Trans).
Nephrolithiasis.
Identify (from Radio Lab Trans).
Ureterolithiasis, left
Identify (from Radio Lab Trans).
Cystolithiasis.
Calcific density floating within the bladder.
Identify (from Radio Lab Trans).
Hydronephrosis.
Identify (from Radio Lab Trans).
Hydronephrosis.
Identify (from Radio Lab Trans).
Ureteral obstruction secondary to fibrosis. Note: dilation proximal to stricture.
Identify (from Radio Lab Trans).
Renal tuberculosis.
Identify (from Radio Lab Trans).
Bacterial pyelonephritis with abscess formation.
Identify (from Radio Lab Trans).
Bacterial pyelonephritis.
Infected and swollen kidney
Notes:
Not all large kidneys are compensating/hypertrophied kidneys or masses, consider
edema. R kidney is edematous and seen to be almost touching the anterior
abdominal wall
Identify (from Radio Lab Trans).
Transitional cell carcinoma of the renal pelvis.
Notes: looks homogenous, and seems to be growing upward
Identify (from Radio Lab Trans).
Renal carcinoma (MRI).
Note: the whole thing is the mass.
Identify (from Radio Lab Trans).
Renal Carcinoma (MRI).
Identify (from Radio Lab Trans).
Bilateral Wilm’s Tumor.
Identify (from Radio Lab Trans).
Hematoma surrounding the bladder.
Identify (from Radio Lab Trans).
Urinary bladder CA (MRI).
Familiarize on scout film.
Psoas line, kidney shadow.
- R kidney: smaller and lower
- L kidney: larger and higher
Make sure kidneys are intact, check for
hematomas, retroperitoneal opacities,
obstruction of the psoas line
Plain KUB film -> Nephrogram Phase (3 mins) ->Pyelogram phase (5 mins)->Bladder filling (10 mins)->full bladder film -> Post-void film
Identify (from Radio Lab Trans).
Enlarged prostate (UTZ)
Note: see protrusion into bladder.
Identify (from Radio Lab Trans).
Cystitis (UTZ).
Identify (from 2015 reviewer).
Acute pyelonephritis (gross).
Identify (from 2015 reviewer).
Papillary necrosis (gross).
Identify (from 2015 reviewer).
Chronic pyelonephritis (gross).
Identify (from 2015 reviewer).
Chronic pyelonephritis (LM).
Identify (from 2015 reviewer).
Chronic pyelonephritis.
Note thyroidization
Identify (from 2015 reviewer).
Benign nephrosclerosis (gross).
Identify (from 2015 reviewer).
Benign nephrosclerosis (LM).
Identify (from 2015 reviewer).
Benign nephrosclerosis (LM).
Identify (from 2015 reviewer).
Benign nephrosclerosis.
Identify (from 2015 reviewer).
Malignant hypertension (gross).
Note: FLEA-BITTEN appearance (due to petechial hemorrhages).
Identify (from 2015 reviewer).
Malignant hypertension (LM).
Note: ONION-SKIN APPEARANCE due to layering of collagen.
Identify (from 2015 reviewer).
Malignant hypertension (LM).
Onion-skin appearance.
Identify (from 2015 reviewer).
Renal infarct.
Identify (from 2015 reviewer).
Angiomyolipoma (gross).
Identify (from 2015 reviewer).
Angiomyolipoma.
Identify (from 2015 reviewer).
Oncocytoma (gross).
Identify (from 2015 reviewer).
Oncocytoma (LM).
Identify (from 2015 reviewer).
Oncocytoma.
Identify (from 2015 reviewer).
Collecting duct/Bellini duct carcinoma.
Identify (from 2015 reviewer).
Sarcomatoid renal cell carcinoma.
Identify (from 2015 reviewer).
Papillary urothelial carcinoma of the renal pelvis.
Identify (from 2015 reviewer).
Wilm’s tumor (LM).
Identify (from 2015 reviewer).
Urothelial papilloma, LM (LPO).
Identify (from 2015 reviewer).
Urothelial papilloma, LM.
Identify (from 2015 reviewer).
Papillary urothelial neoplasm of low malignant potential (PUNLMP).
Identify (from 2015 reviewer).
PUNLMP.
Identify (from 2015 reviewer).
Low grade papillary urothelial carcinoma.
Identify (from 2015 reviewer).
High grade papillary urothelial carcinoma.
Identify (from 2015 reviewer).
Carcinoma in situ (flat urothelial carcinoma).
Note: only urothelium will be affected.
Identify (from 2015 reviewer).
Invasive urothelial cancer (gross).
Identify (from 2015 reviewer).
Invasive urothelial cancer.
Identify (from 2015 reviewer).
Squamous cell CA of the bladder.
Identify (from 2015 reviewer).
Leiomyoma (mesenchymal tumor of the bladder).
Identify (from 2015 reviewer).
Leiomyosarcoma.
Identify (from 2015 reviewer).
Embryonal rhabdomyosarcoma.
Identify (from 2015 reviewer).
Benign prostatic hyperplasia.
Identify (from 2015 reviewer).
Benign prostatic hyperplasia (LM).
Identify (from 2015 reviewer).
Benign prostatic hyperplasia.
Identify (from 2015 reviewer).
Benign prostatic hyperplasia.
MEMORIZE!
Prostatic adeno CA (from 2015 reviewer).
Gleason score?
Gleason 2.
Prostatic adeno CA (from 2015 reviewer).
Gleason score?
Gleason 3.
Prostatic adeno CA (from 2015 reviewer).
Gleason score?
Gleason 4.
Prostatic adeno CA (from 2015 reviewer).
Gleason score?
Gleason 5.
Identify (from 2015 reviewer).
Prostatic adenoCA with crystalloids.
Identify.
Dysmorphic RBCs with some normal RBCs.
(Normal RBCs: > 10 per HPF)
Identify the pointed structures.
PMN cells.
Neutrophils: glitter cells
Identify.
Benign tubular epithelial cells.
Identify.
Benign transitional epithelial cells from bladder.
L: w/o stain
R: w/ stain
Identify the structure and what it indicates.
Oval fat body with Maltese Cross appearance.
Indicates nephrosis.
Identify.
Yeast exhibiting budding + crenated RBC
Type of cast
RBC casts
Type of cast. Also identify the pointed structures.
WBC casts (also called glitter cells) stuck together by
Tamm Horsfall protein (pointed)
Type of cast
Granular cast
Type of cast
Hyaline cast (consists almost entirely of Tamm Horsfall protein)
Type of cast and what it indicates
Waxy cast
-represents urine stasis or CRF
Type of cast
Fatty cast
- associated with nephrotic syndrome, toxic tubular necrosis, DM, and crash injuries
- may consist of multiple Maltese crosses
Type of crystal and identify if normal/abnormal
Calcium oxalate crystals. Normal.
Type of crystal and identify if normal/abnormal
Triple phosphate crystals. Normal.
“Coffin lid appearance”
Signifies alkaline pH
Type of crystal and identify if normal/abnormal.
Urate crystals. Normal.
Most commonly seen as AMORPHOUS urates,
uric acid, acid urates, and sodium urates.
Type of crystal and identify if normal/abnormal.
Tyrosine crystals. ABNORMAL.
Associated with LIVER DISORDERS.
Type of crystal and identify if normal/abnormal
Cystine crystals. ABNORMAL.
Associated with hereditary cystinuria.
Type of crystal and identify if normal/abnormal
Ammonium biurate crystals. Normal.
Yellow brown crystals. “Thorny apple”
Type of crystal and identify if normal/abnormal
Cholesterol crystals. ABNORMAL.
Colorless rectangular with notched edges/plates
Lipiduria-like nephrotic sydrome
