Nephrology Picture Diagnosis Flashcards
ATN (acute tubular necrosis)
hydronephrosis
pyelonephritis
- WBC cast
“Maltese cross” appearance of oval fat bodies seen in nephrotic syndrome
hydronephrosis
hydronephrosis
dysmorphic erythrocytes (“Mickey Mouse” ears appearance)
fundoscopic examination indicating hypertensive retinopathy
- white arrows = generalized arteriolar narrowing
- black arrows = compared with venule diameter
peaked T waves characteristic of hyperkalemia
hypocalcemia
erythrocyte cast indicative of glomerular disease
urenic frost
calcium oxalate DIhydrate crystals
- envelope-shaped
- associated with hyperoxaluria and calcium oxalate stone formation
leukocytes in setting of UTI
ADPKD
ADPKD
- hypokalemia
- initially, T waves decrease in amplitude
- ST segment flattens
- then U waves appear after the T waves
- the U waves ultimately replace the T waves completely
- this may give the impression of QT prolongation, but it is really a QU interval
tuberous sclerosis
angiokeratomas in Fabry disease
“storiform” pattern seen in IgG4-related disease
granular casts suggestive of acute tubular necrosis (ATN)
isomorphic RBCs
crenated RBCs
dysmorphic RBCs
budding yeast
lipid droplets
WBCs
renal tubular epithelial (RTE) cells
hyaline casts
RTE cell cast
RBC cast
WBC casts
granular casts
uric acid crystals
calcium oxalate cystals (monohydrate)
- “dumbell” shape
acyclovir crystals
granular casts (muddy brown casts) suggestive of ATN
granular casts
- Effacement of proximal tubule cells
- Loss of brush border
- Patchy loss of tubular cells
- Focal tubule dilation
- Tubular casts
- Areas of cellular regeneration in recovery
osmotic nephrosis
diabetic nephropathy
- Kimmelstiel-Wilson nodules (arrows)
IgA nephropathy
IgA nephropathy
minimal change disease
- foot process effacement
advanced FSGS
C1q nephropathy
dense deposit disease
C3 glomerulopathy
membranous nephropathy
- Jones silver stain
- small spike-like projections
membranoproliferative glomerulonephritis (MPGN)
- diffuse endocapillary hypercellularity
- looks lobular
- PAS stain
membranoproliferative glomerulonephritis (MPGN)
- diffuse endocapillary hypercellularity
- extensive duplication of GBM
- Jones silver stain
MPGN
- IF
- smooth outline of sausage-shaped, chunky peripheral loop deposits and scattered mesagnial deposits
fibrillary GN
- LM pattern varies
- this case shows moderate mesangial proliferation and occasional BM double contours
- Jones silver stain
fibrillary GN
- may be lobular or nodular proliferative pattern, which may resemble diabetic nephropathy
- PAS stain
acute postinfectious GN
- C3 positivity
- predominant starry-sky pattern
- more elongated deposits, “garland pattern” (bottom)
- anti-C3 IF x 400
IgA nephropathy
- crescentic injury
IgA nephropathy
- predominantly mesangial pattern
- anti-IgA IF x 400
light chain deposition disease (LCDD)
- minimal mesangial expansion
- mild increase in mesangial cellularity and matrix
- specific dx made by IF and confirmed by EM
light chain deposition disease (LCDD)
- characteristic nodular appearance
- may be difficult to distinguish from diabetic nephropathy, BUT BM not as prominent
- need IF and EM to confirm dx
light chain deposition disease (LCDD)
- kappa monoclonal light chain staining tubular basement membranes
- anti-kappa IF x 100
light chain deposition disease (LCDD)
- finely granular deposits found along internal aspect of GBM
- EM x 11,250
light chain deposition disease (LCDD)
- granular deposits found along internal aspect of GBM
- EM x 40,000
- light and heavy chain deposition disease (LHCDD)
- membranoproliferative pattern w/ increased mesangial cells and matrix
- confirmed by IF and EM
- Jones silver stain, x 400
- light and heavy chain deposition disease (LHCDD)
- nodular glomerulosclerosis, INDISTINGUISHABLE from LCDD on LM
- confirmed by IF and EM
- Jones silver stain, x 200
- light and heavy chain deposition disease (LHCDD)
- strong glomerular capillary loop and mesangial staining in a smudgy, continuous pattern along GBM
- also tubular BM staining (left)
- anti-IgG IF, x 400
light and heavy chain deposition disease (LHCDD)
- subendothelial and subepithelial deposits
- coarsely fibrillar substructure
light and heavy chain deposition disease (LHCDD)
- frequent tubular BM deposits
- EM, x 25,625
amyloidosis
- segmental amorphous, eosinophilic, fluffy “cotton candy” in mesangium
amyloidosis
- massive amyloid deposits in glomeruli and arterioles
- nodular appearance d/t amorphous, acellular eosinophilic pale material
- H&E, x 100
amyloidosis
- apple-green birefringence w/ Congo red stain and viewed under polarized light
HIV-associated nephropathy (HIVAN)
- microcystic tubular injury and collapse of glomerular tuft
HIV-associated nephropathy (HIVAN)
- glomerulus w/ collapsing form of injury
sickle cell nephropathy
- massive sludging of RBCs
- H&E, x 100
sickle cell nephropathy
- sickling causing congestion in glomerulus and peritubular capillaries
- H&E, x 100
sickle cell nephropathy
- capillary loop greatly distorted d/t swollen endothelial cells and interposition w/o well-defined immune complexes
Fabry disease
- vacuolated, honeycomb appearance
- results from accumulation of abnormal glycosphingolipid in Fabry disease
Fabry disease
- lysosomal inclusions and myelin bodies, especially in podocytes
- toluidine blue-stained
Fabry disease
- myelin bodies and lysosomal inclusions, some of which are lamellated
Fabry disease
- lysosomal inclusion w/ myelin body appearance in the podocyte
Fabry disease
- lysosomal inclusions w/ lamellated structure
- “zebra bodies”
lipoprotein glomerulopathy
- massive intraluminal pale lipid thrombi in glomerular capillaries
lipoprotein glomerulopathy
- intracapillary thrombi stain brightly positive for lipid
- oil red O stain, x 200
lecithin-cholesterol acyltransferase (LCAT) deficiency
- focal prominent endocapillary foam cell infiltration
- PAS, x 200
- lecithin-cholesterol acyltransferase (LCAT) deficiency
- numerous lipid inclusion seen w/i intracapillary foam cells
- EM, x 8000
- minimal change disease
- normal LM
- diffuse effacement of foot processes by EM
focal segmental glomerulosclerosis
- sharply defined segmental sclerosis
- obliteration of capillary loops
- increased matrix
- no deposits
- diffuse foot process effacement by EM
collapsing glomerulopathy
- segmental or global collapse of capillary tuft w/ overlying visceral epithelial cell hyperplasia
- no deposits
focal segmental glomerulosclerosis, tip lesion
- segmental sclerosis confined to proximal tubular pole
- often has endocapillary hypercellularity w/ foam cells and overlying visceral epithelial cell hyperplasia
- foot processes diffusely and globally effaced, even in glomeruli and segments w/o the tip lesions
- no deposits
dense deposit disease
- membranoproliferative pattern
- endocapillary hypercellularity and glomerular basement membrane double contours
- GBM is altered by dense deposits in a ribbon-like pattern, w/ mesangial dense material as well
membranous nephropathy
- no evident proliferation by LM
- global subepithelial deposits (may be seen by LM) by GBM spike reaction on silver stain
membranous nephropathy
- in earliest stages, deposits do not stain w/ silver may be seen in tangential sections as holes, producing a corkboard appearance
membranous nephropathy
- early basement membrane reaction develops, visualized as small spikes on silver stain
membranous nephropathy
- basement membrane reaction may encircle deposits, w/ ensuing double contours and a ladder-type appearance on silver stain
membranous nephropathy
- in far advanced cases, deposits may become partially resorbed, leaving a rarefied area of the GBM as seen by EM
membranoproliferative glomerulonephritis (MPGN)
- endocapillary proliferation/hypercellularity and GBM double contours
- d/t mesangial and subendothelial deposits, w/ resultant interposition and new basement membrane being laid down, causing the “split” appearance
membranoproliferative glomerulonephritis (MPGN)
- in the early stages, only mesangial and enocapillary hypercellularity may be seen by LM, w/o GBM reaction yet
membranoproliferative glomerulonephritis (MPGN)
- interposed cells, both monocytes/macrophages and mesangial cells, migrating in between the GBM and endothelium, present in response to subendothelial depositis
membranoproliferative glomerulonephritis (MPGN)
- interposed cells and new GBM reaction devlop in response to the subendothelial deposits
- these cells and deposits do NOT stain w/ silver, and thus the capillary wall has a double contour “TRAM-TRACK” appearance
acute postinfectious glomerulonephritis
- exudative hypercellularity w/ numerous polymorphonuclear leukocytes and endocapillary hypercellularity
- scattered mesangial and large hump-shaped subendothelial deposits
IgA nephropathy
- mesangial cell and matrix increase
- mesangial deposits
K V5M1 Q 68
AMR
This patient with progressive allograft dysfunction, proteinuria, and donor-specific HLA antibody (DSA) has chronic active antibody-mediated rejection (AMR). This diagnosis is confirmed by allograft biopsy findings of peritubular capillary and glomerular C4d staining. In addition, glomerulitis and GBM double contours are present (arrows) and indicate transplant glomerulopathy, a common feature of chronic AMR.
The Banff criteria for the diagnosis of chronic active AMR include all of the following:
- Evidence of chronic tissue injury including transplant glomerulopathy.
- Evidence of current or recent antibody interaction with vascular endothelium including C4d staining in the peritubular capillaries, microvascular inflammation including glomerulitis and peritubular capillaritis, or increased expression of gene transcripts associated with AMR.
- Presence of HLA or non-HLA DSAs.
