Nephrology Picture Diagnosis Flashcards

1
Q
A

ATN (acute tubular necrosis)

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2
Q
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hydronephrosis

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3
Q
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pyelonephritis

  • WBC cast
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4
Q
A

“Maltese cross” appearance of oval fat bodies seen in nephrotic syndrome

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5
Q
A

hydronephrosis

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6
Q
A

hydronephrosis

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7
Q
A

dysmorphic erythrocytes (“Mickey Mouse” ears appearance)

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8
Q
A

fundoscopic examination indicating hypertensive retinopathy

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9
Q
A
  • white arrows = generalized arteriolar narrowing
  • black arrows = compared with venule diameter
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10
Q
A

peaked T waves characteristic of hyperkalemia

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11
Q
A

hypocalcemia

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12
Q
A

erythrocyte cast indicative of glomerular disease

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13
Q
A

urenic frost

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14
Q
A

calcium oxalate DIhydrate crystals

  • envelope-shaped
  • associated with hyperoxaluria and calcium oxalate stone formation
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15
Q
A

leukocytes in setting of UTI

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16
Q
A

ADPKD

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17
Q
A

ADPKD

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18
Q
A
  • 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
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19
Q
A

tuberous sclerosis

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20
Q
A

angiokeratomas in Fabry disease

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21
Q
A

“storiform” pattern seen in IgG4-related disease

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22
Q
A

granular casts suggestive of acute tubular necrosis (ATN)

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23
Q
A

isomorphic RBCs

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24
Q
A

crenated RBCs

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25
Q
A

dysmorphic RBCs

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26
Q
A

budding yeast

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27
Q
A

lipid droplets

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28
Q
A

WBCs

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29
Q
A

renal tubular epithelial (RTE) cells

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30
Q
A

hyaline casts

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31
Q
A

RTE cell cast

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32
Q
A

RBC cast

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33
Q
A

WBC casts

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34
Q
A

granular casts

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35
Q
A

uric acid crystals

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36
Q
A

calcium oxalate cystals (monohydrate)

  • “dumbell” shape
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37
Q
A

acyclovir crystals

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38
Q
A

granular casts (muddy brown casts) suggestive of ATN

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39
Q
A

granular casts

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40
Q
A
  • 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
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41
Q
A

osmotic nephrosis

42
Q
A

diabetic nephropathy

  • Kimmelstiel-Wilson nodules (arrows)
43
Q
A

IgA nephropathy

44
Q
A

IgA nephropathy

45
Q
A

minimal change disease

  • foot process effacement
46
Q
A

advanced FSGS

47
Q
A

C1q nephropathy

48
Q
A

dense deposit disease

49
Q
A

C3 glomerulopathy

50
Q
A

membranous nephropathy

  • Jones silver stain
  • small spike-like projections
51
Q
A

membranoproliferative glomerulonephritis (MPGN)

  • diffuse endocapillary hypercellularity
  • looks lobular
  • PAS stain
52
Q
A

membranoproliferative glomerulonephritis (MPGN)

  • diffuse endocapillary hypercellularity
  • extensive duplication of GBM
  • Jones silver stain
53
Q
A

MPGN

  • IF
  • smooth outline of sausage-shaped, chunky peripheral loop deposits and scattered mesagnial deposits
54
Q
A

fibrillary GN

  • LM pattern varies
  • this case shows moderate mesangial proliferation and occasional BM double contours
  • Jones silver stain
55
Q
A

fibrillary GN

  • may be lobular or nodular proliferative pattern, which may resemble diabetic nephropathy
  • PAS stain
56
Q
A

acute postinfectious GN

  • C3 positivity
  • predominant starry-sky pattern
  • more elongated deposits, “garland pattern” (bottom)
  • anti-C3 IF x 400
57
Q
A

IgA nephropathy

  • crescentic injury
58
Q
A

IgA nephropathy

  • predominantly mesangial pattern
  • anti-IgA IF x 400
59
Q
A

light chain deposition disease (LCDD)

  • minimal mesangial expansion
  • mild increase in mesangial cellularity and matrix
  • specific dx made by IF and confirmed by EM
60
Q
A

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
61
Q
A

light chain deposition disease (LCDD)

  • kappa monoclonal light chain staining tubular basement membranes
  • anti-kappa IF x 100
62
Q
A

light chain deposition disease (LCDD)

  • finely granular deposits found along internal aspect of GBM
  • EM x 11,250
63
Q
A

light chain deposition disease (LCDD)

  • granular deposits found along internal aspect of GBM
  • EM x 40,000
64
Q
A
  • 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
65
Q
A
  • light and heavy chain deposition disease (LHCDD)
  • nodular glomerulosclerosis, INDISTINGUISHABLE from LCDD on LM
  • confirmed by IF and EM
  • Jones silver stain, x 200
66
Q
A
  • 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
67
Q
A

light and heavy chain deposition disease (LHCDD)

  • subendothelial and subepithelial deposits
  • coarsely fibrillar substructure
68
Q
A

light and heavy chain deposition disease (LHCDD)

  • frequent tubular BM deposits
  • EM, x 25,625
69
Q
A

amyloidosis

  • segmental amorphous, eosinophilic, fluffy “cotton candy” in mesangium
70
Q
A

amyloidosis

  • massive amyloid deposits in glomeruli and arterioles
  • nodular appearance d/t amorphous, acellular eosinophilic pale material
  • H&E, x 100
71
Q
A

amyloidosis

  • apple-green birefringence w/ Congo red stain and viewed under polarized light
72
Q
A

HIV-associated nephropathy (HIVAN)

  • microcystic tubular injury and collapse of glomerular tuft
73
Q
A

HIV-associated nephropathy (HIVAN)

  • glomerulus w/ collapsing form of injury
74
Q
A

sickle cell nephropathy

  • massive sludging of RBCs
  • H&E, x 100
75
Q
A

sickle cell nephropathy

  • sickling causing congestion in glomerulus and peritubular capillaries
  • H&E, x 100
76
Q
A

sickle cell nephropathy

  • capillary loop greatly distorted d/t swollen endothelial cells and interposition w/o well-defined immune complexes
77
Q
A

Fabry disease

  • vacuolated, honeycomb appearance
  • results from accumulation of abnormal glycosphingolipid in Fabry disease
78
Q
A

Fabry disease

  • lysosomal inclusions and myelin bodies, especially in podocytes
  • toluidine blue-stained
79
Q
A

Fabry disease

  • myelin bodies and lysosomal inclusions, some of which are lamellated
80
Q
A

Fabry disease

  • lysosomal inclusion w/ myelin body appearance in the podocyte
81
Q
A

Fabry disease

  • lysosomal inclusions w/ lamellated structure
  • “zebra bodies”
82
Q
A

lipoprotein glomerulopathy

  • massive intraluminal pale lipid thrombi in glomerular capillaries
83
Q
A

lipoprotein glomerulopathy

  • intracapillary thrombi stain brightly positive for lipid
  • oil red O stain, x 200
84
Q
A

lecithin-cholesterol acyltransferase (LCAT) deficiency

  • focal prominent endocapillary foam cell infiltration
  • PAS, x 200
85
Q
A
  • lecithin-cholesterol acyltransferase (LCAT) deficiency
  • numerous lipid inclusion seen w/i intracapillary foam cells
  • EM, x 8000
86
Q
A
  • minimal change disease
  • normal LM
  • diffuse effacement of foot processes by EM
87
Q
A

focal segmental glomerulosclerosis

  • sharply defined segmental sclerosis
  • obliteration of capillary loops
  • increased matrix
  • no deposits
  • diffuse foot process effacement by EM
88
Q
A

collapsing glomerulopathy

  • segmental or global collapse of capillary tuft w/ overlying visceral epithelial cell hyperplasia
  • no deposits
89
Q
A

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
90
Q
A

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
91
Q
A

membranous nephropathy

  • no evident proliferation by LM
  • global subepithelial deposits (may be seen by LM) by GBM spike reaction on silver stain
92
Q
A

membranous nephropathy

  • in earliest stages, deposits do not stain w/ silver may be seen in tangential sections as holes, producing a corkboard appearance
93
Q
A

membranous nephropathy

  • early basement membrane reaction develops, visualized as small spikes on silver stain
94
Q
A

membranous nephropathy

  • basement membrane reaction may encircle deposits, w/ ensuing double contours and a ladder-type appearance on silver stain
95
Q
A

membranous nephropathy

  • in far advanced cases, deposits may become partially resorbed, leaving a rarefied area of the GBM as seen by EM
96
Q
A

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
97
Q
A

membranoproliferative glomerulonephritis (MPGN)

  • in the early stages, only mesangial and enocapillary hypercellularity may be seen by LM, w/o GBM reaction yet
98
Q
A

membranoproliferative glomerulonephritis (MPGN)

  • interposed cells, both monocytes/macrophages and mesangial cells, migrating in between the GBM and endothelium, present in response to subendothelial depositis
99
Q
A
100
Q
A

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
101
Q
A

acute postinfectious glomerulonephritis

  • exudative hypercellularity w/ numerous polymorphonuclear leukocytes and endocapillary hypercellularity
  • scattered mesangial and large hump-shaped subendothelial deposits
102
Q
A

IgA nephropathy

  • mesangial cell and matrix increase
  • mesangial deposits