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S4M2 > Renal Path > Flashcards

Renal Path Flashcards

1
Q

If you see red cell casts, where is the blood coming from?

A

Glomerulous

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2
Q

If you see cellular casts, what has happened?

A

Acute Tubular Necrosis

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3
Q

What if you see granular casts?

A

Meh. Less specific.. could be tubular cells, white cells….

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4
Q

What’s this?

A

Red Cell Cast

Indicates Nephritic Syndrome

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5
Q

What is this?

What does it mean?

A

White cell cast

Indicates Infection in kidney (because formed cast)

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6
Q

What’s this?

What does it mean?

A

Lipid cast (with characteristic maltese cross)

Indicates Nephrotic Syndrome

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7
Q

What’s this?

What does it mean?

A

Epithelial cell cast

Indicates Acute Tubular Necrosis

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8
Q

What might it mean to see broad casts?

A

Probably Chronic Renal Failure

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9
Q

Azotemia vs Uremia

A

Azotemia = Increased BUN & Creatinine without disease

Uremia = same, but with disease. can affect any organ

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10
Q

What are the different causes of azotemia or acute renal failure?

A
  1. Pre-renal
  2. Renal
  3. Post-renal
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11
Q

BUN:Creatinine is >20:1

What is your dx?

A

Pre-renal Failure

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12
Q

Causes of Acute Pre-Renal Failure?

A

Sudden hypotension

Decreased perfusion

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13
Q

What is Nephritic Syndrome?

A

Renal failure with red cell casts

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14
Q

What is Rapidly Progressive Glomerulonephritis?

A

Nephritic Syndrome + Acute Renal Failure

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15
Q

What is the most common cause of nephritic syndrome?

A

Post-strep Glomerulonephritis

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16
Q

Cuases of Rapidly Progressive Glomerulo-Nephritis?

A
  1. Anti-GBM
    • Goodpasture)
  2. Immune Complex
    • Post-infx
    • SLE
    • H-S purpura/IgA nephropathy)
  3. ANCA-Associated (aka *pauci-immune *- don’t see anything on immunofluorescence)
    • Wegener’s granulomatosis
    • Microscopic angiitis
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17
Q

Why do you get edema in nephrotic syndrome?

A

Lose a lot of protein, albumin decreases with it.

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18
Q

Why do you get hyperlipidemia in nephrotic syndrome?

A

Liver makes more lipoprotein – trying to compensate for low protein

Will cause lipid cast formation

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19
Q

What if you see lots of eosinophils in a cast?

A

Probably drug reaction (Acute Intersitial Nephritis)

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20
Q

In what condition do you lose Foot Processes (F)?

A

Anything with Nephrotic Syndrome

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21
Q

How is it that you can sometimes get hematuria but not proteinuria?

A

Complex charges (basement mem has GAGs that are negatively charged– keep out proteins)

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22
Q

What stain is this?

What does it show?

A

Silver stain– shows membranes

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23
Q

What is this? What does it show?

A

Immunofluorescence– shows immune deposits

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24
Q

Types of Glomerulonephritis

A

Global: Entire glomerulus

Segmental: Part of glomerulus

Diffuse: >50% of glomeruli are affected

Focal:

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25
Q

Where can immune complexes be depositied in Glomerulonephritis?

A

Subepithelial (large or small)

Subendothelial

Mesangial

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26
Q

What disease & why?

A

Diabetic Nephropathy

  • thickened GBM
  • thickened arterioles
  • Arteriosclerosis
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27
Q

What would urine show in patients with Diabetic Nephropathy?

A

Proteinuria

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28
Q

What are the key morpholic features of diabetic nephropathy?

A
  • Thick GBM
  • Mesangial sclerosis
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29
Q

What pattern of sclerosis is pretty specific for Diabetes?

A

Nodular Glomerulosclerosis

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30
Q

What are two diseases that can cause this?

A

Diabetes

HTN

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31
Q

What is a complication of diabetes in the kidney?

A

Infection (pyelonephritis w/ papillary necrosis) due to decreased neutrophil/macrophage function and poor vascular supply

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32
Q

Presentation of Renal Amylodosis?

A

Proteinuria, then nephrotic syndrome

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33
Q

How can you distinguish amyloidosis from diabetic nephropathy?

A

Congo Red Stain

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34
Q

What’s this?

A

amyloidosis

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35
Q

What are the two main causes of amyloidosis?

A
  • Monoclonal lymphoproliferative diseases (multiple myeloma) - AL
  • Chronic inflammatory states - AA
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36
Q

Class II Lupus

A

Mesangioproliferative - like IgA

Hematuria, proteinuria

BUT has full house immunofluorescence

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37
Q

Lupus Classes III & IV are like what?

A

Membranoproliferative or Post-Infectious (Acute Proliferative) GN

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38
Q

How to you distinguish Lupus Class V (Membranous Glomerulonephritis) from Idiopathic Membranous?

A

Full house immunofluorscence with Lupus

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39
Q

Where are the deposits in Class II Lupus?

A

Mainly mesangial

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40
Q

Lupus Nephritis class IV

A

Hypercellular

Diffuse proliferative

Nephrititc, aggressive

Segmental necrosis

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41
Q

Lupus Class V histo

A

Spikes!

No inflamm infiltrate

Advanced sclerosis

Subepithelial intramembranous immune deposits

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42
Q

Linear Immune Deposits

A

Anti-GBM disease:

Abs attacking glomerular BM

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43
Q

Antigen-Antibody complexes most likely get caught WHERE?

A

Subendothelial (classically, with Lupus)

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44
Q

Nephritic syndrome– what will glomerulus look like?

A

Hypercellular (usually inflammatory)

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45
Q

Rapidly Progressive Glomerulo-Nephritis (RPGN)

What would you expect to see?

A

Crescents

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46
Q

Blood in urine. Otherwise healthy. Do biopsy, see this:

A

Mesangial Hypercellularity – IgA Nephropathy

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47
Q
A

IgA Nephropathy / Berger Disease

IF: granular mesangial IgA deposition

LM: Mesangial expansion w/segmental sclerosis

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48
Q

IgA nephropathy + vasculitis = ?

A

Henoch-Schonlein Purpura

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49
Q

Celiac disease– what type of immune nephropathy might you see?

A

IgA

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50
Q

Rapidly Progressive GN = ?

A

Nephritic Syndrome + Acute Renal Failure

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51
Q

What is this and what disease?

A

Crescents

Rapidly Progressive Glomerulonephritis

(would also see large disruptions/gaps in BM)

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52
Q

Anti-GBM: key feature in LM & IF?

A
  • Linear IgG*
  • Crescents*
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53
Q

Post-Infectious GN with crescents: good or bad sign?

A

Bad

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54
Q

RPGN with crescents + vasculitis

A

Pausi-Immune (negative IF)

ANCA present in serum!

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55
Q

Where do you see this?

A

Linear IgG

Anti-GBM disease, diabetes, Goodpasture Synd

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56
Q

Can Pausi-immune associated vasculitis affect other organs besides kidneys?

A

Yes– could be Wegener’s or Polyarteritis Nodosa

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57
Q

What is the classic cause of Nephritic Syndrome?

A

Post-strep (post-infectious)

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58
Q

Nephritic syndrome: main histologic feature

What will IM show?

A

Hypercellularity of neutrophils

IM: Granular- huge subepithelial deposits

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59
Q

Agressive Post-Strep Glomerulonephritis would show what histology?

A

Crescents

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60
Q

Nephrotic Syndrome: What will you always see on EM?

A

“Loss” of foot processes

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61
Q

Nephrotic Syndrome: Minimal Change

  • demographics
  • what will you see by LM? IF?
A

Kids

Normal LM and IF. (Can only see in EM)

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62
Q

Focal Segmental Glomerulosclerosis:

What will you see by LM? IF?
Prognosis?
Clinical S/S?

A

LM: Focal segmental scarring (can be missed by small bx– will look like minimal change)

IF: Negative

Prognosis: poorer than minimal change

Clinical S/S: hematuria + hypertension

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63
Q

Nephrotic Syndrome: IF shows peripheral granular IgG– what are your first thoughts?

A

Membranous (others don’t show IF change)

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64
Q

Fatty Casts on urinalysis?

A

Nephrotic Syndrome

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65
Q

How much proteinuria is needed to be diagnostic of Nephrotic Syndrome?

A

>3.5 g/day

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66
Q

Focal Segmental Glomerulosclerosis, see this:

A

Collapsing glomerulopathy

poor prognosis

associated with HIV

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67
Q

See this:

A

Membranous Glomeronephritis (stage 2)

(BM growing up between deposits)

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68
Q

Lots of proteinuria & hematuria.

Disease?

H&E?

A
  • *Membranoproliferative**: hypercellular, lobulated morphology
  • poor prognosis :(
  • *Double contours** on BM stain (caused by mesangial cell interposition & immune deposits splitting BM)
  • indicative of type I
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69
Q

Type II Membranoproliferative Glomerulonephritis:

histo

serum marker?

A

Entire glomerular BM is one large dense deposit

C3 Neprhitic Factor in blood!! (keep complement activated)

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70
Q

Biposy of renal failure: scarred glomeruli = ?

A

Chronic glomerulonephritis

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71
Q

What is it?

Caused by?

Pathogenesis?

A

Flea bitten kidney + Fibrinoid necrosis

Caused by Malignant HTN

Ischemia of glomeruli -> RAS activation -> further HTN -> further injury

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72
Q
A

Onion skin Hyperplastic Arteriosclerosis

Long standing malignant HTN

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73
Q

Malignant HTN caused by which kidney?

A

Little one (renal artery stenosis)

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74
Q

What group of diseases show little thrombi all over the glomerulus?

3 main causes?

A

Thrombotic Microangiopathies:

  • Hemolytic-Uremic Syndrom (HUS)
  • Atypical HUS
  • Thrombotic Thrombocytopenia
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75
Q

What causes HUS?

A

Infection of intestinal bacteria (usually E.coli)

toxin (Shiga-like toxin) injure endothelial cells

Present with flu/diarrhea followed by bleeding issues

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76
Q

What causes Atypical HUS?

A

Hyperactive immunity- can’t turn off complement

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77
Q

What causes Thrombotic Thrombocytopenia?

A

Functional deficiency of ADAMTS13

causes platelet aggregates (can’t sufficiently cleave VWF)

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78
Q
A

Hydronephrosis:

caused by obstruction, reflux

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79
Q

Dx? Cause?

A

Hydronephrosis caused by reflux

80
Q
A

Acute tubular necrosis

Epithlelial cell cast

Can be ischemic or toxic

Good prognosis if you get eliminate the causeNext >>

81
Q
A

Normal

82
Q

Dx? Presentation?

A

Alport Syndrome- multi-layered lamina densa

Present with hematuria, proteinura, hearing loss, vision prob

83
Q
A

Thin Basement Membrane Disease

good prognosis (normal fx)

84
Q
A

Renal Dysplasia- very cystic, show cartilage

benign, associated with other congential defects

85
Q
A

AD-PDK

in adults, common

can get Berry Aneurysm

86
Q
A

AR-PKD

kids, rare

87
Q

Significance?

A

Dialysis-Assoc: some incr. risk for renal failure

Simple: meh. no.

88
Q
  1. What’s this?
    What would IF look like?
  2. What’s this?
    What would they have in the blood?
  3. What’s this?
A
  1. Large sub-epithelial hump
    * IF*: granular
  2. Dense Deposit Disease (MPGN 2)
    * Serum*: C3 Nephritic Factor
  3. Subendothelial Deposit (Lupus)
89
Q

What’s this?

Presentation?

A

IgA nephropathy

Mesangial prolif- mesangial IgA

Present with hematuria

90
Q
A

Crescents - BAD prognosis

91
Q

Prognosis? Other organs affected?

A

Anti-GBM disease

LM: Crescentic glomerulonephritis

IF: linear

Bad prog

Can affect Lung

92
Q

Dx? What’s in serum?

A

Crescentic Glomerulonephritis with Vasculitis

(Pauci-Immune)

ANCA in blood!

93
Q
A

Hypercellular neutrophils. Post-infectious

More in kids

good prognosis

Granular IgG & C3 deposits

94
Q
A

Large cellular glomeruli with neutrophils. Humps seen on right.

Post-infectious

95
Q
A

Minimal change disease

Normal LM

IF negative

Loss of foot processes

96
Q
A

Focal Segmental Glomerulosclerosis

97
Q
A

1: small subepithelial deposits

98
Q
A

2: BM starting to grow up between deposits (spikes)

99
Q
A

spikes = Stage 2 Membranous

100
Q
A

Stage 3:

IF: “STRING OF PEARLS”– peripheral granular

101
Q

Stage? Presentation of membranous?

A

4: thick membrane, few deposits

Present with Nephrotic Synd (proteinuria)

Can be seen w/ Lupus class V

102
Q
A

Membranous GN

103
Q
A

Stage 3- peripheral granular

104
Q
A

Membranoproliferative Stage 1

105
Q
A

Mesangial expansion into BM–

Membranoproliferative GN type 1

106
Q
A

Type 2 Membranoproliferative

large dense glomerulus

107
Q
A

C3 Nephritic Factor

108
Q
  • Minimal Change:
  • Membranous:
  • Lupus
  • IgA: where are the deposits?
  • T
  • Type 2 MPGN?
  • Post-Infectious
  • Lupus deposits at?
  • Amyloid deposited at?
  • Amyloid appearance?
  • 2 types of amyloid?
  • Diseases with amyloid?
  • Diabetes EM?
  • Thin Basement Membrane Dis
A

EM:

  • Minimal Change: Foot Process obliteration
  • Membranous: Subepithelial deposits, spikes by LM
  • Lupus: Mesangial deposits
  • IgA: Mesangial deposits
  • Type 1 MPGN: mesangium, subendothelial
  • Type 2 MPGN: one large density
  • Post-Infectious: huge subepithelial humps
  • Amyloid: BM, mesangial deposits; skinny fibrils
    • 2 types: light chain (AL), chronic inflamm (AA)
    • Diseases assoc: Myeloma, Lymphoma, autoimmune
  • Diabetes: Very thick GBM, no deposits
  • Thin Basement Membrane Dz: Thin BM
109
Q
A

Diabetic Nephropathy:

very thick GBM, arteriosclerosis

110
Q
A

Thick GBM

111
Q
A

Mesangial sclerosis + thick GBM

112
Q
A

Nodular Glomerulosclerosis seen in Diabetes

113
Q
A

Arteriosclerosis:

Benign HTN, diabetes

114
Q
A

Papillary Necrosis

caused by:

  1. Pyelonephritis + Diabetes
  2. Pyelonephritis + Obstruction
  3. Analgesic Nephropathy
115
Q
A

Amyloidosis or Diabetes

116
Q
A

Amyloid

117
Q

Class? Presentation? Differential?

A

Class 2: mesangial proliferation only

Present with hematuria

Looks like IgA nephropathy but full house IF

118
Q

Type? Presentation? Differential?

A

Type 3: focal proliferative

Present with Nephritic Syndrome

Like Membranoproliferative but full house IF

119
Q

Almost all glomeruli look like this.

Class?

A

Lupus Nephritis Class 4

120
Q
A

class 4

121
Q

Class?

Presentation?

Differential?

A

Class V: membranous

Present as Nephrotic

Looks like Idiopathic Membranous GN Full house IF

122
Q
A

Benign HTN

arteriosclerosis– granular appearance

Also can be caused by diabetes

123
Q
A

Malignant HTN

Arteriolar Necrosis, petichial hemorrhage, onion skin arterioles

124
Q
A

Little one (hypoperfused, increases renin)

125
Q

Dx? Causes?

A

Thrombotic Microangiopathy

Caused by:
TTP: no ADAMTS13 (cleaves vWF)
HUS (food poisoing- toxin damages endoth cells)
Atypical HUS (Factor H)

126
Q
A

Pyelonephritis

usually from cystitis (ascending)
Fecal flora

can also be from hematogenous spread

127
Q
A

Papillary Necrosis

  • Analgesic Nephropathy + Diabetes
  • Pyelonephritis + Diabetes
  • Pyelonephritis + Obstruction
128
Q
A

Chronic Pyelonephritis

blunted calices

2 main causes: obstruction, reflux
Obstruction - diffuse
Reflux- @ poles

129
Q
A

Xanthogranulomatous Pyelonephritis

can look like renal cell carinoma

usually from Proteus

130
Q

Dx? Cause? Urinalysis?

A

Drug-Induced Interstitial Nephritis

NSAIDs, diuretics, abx…

Eosinophil cast

131
Q
A

Meyloma Light Chain casts

132
Q
A

Clear Cell Renal Cell Ca

assoc w/VHL mutation

133
Q
A

Sarcomatoid Renal Cell CA

bad prognosis

134
Q
A

Renal Vein invasion

135
Q
A

Oncocytoma

Scar
Granular eosinophilic cells
Mitochondria

Benign

136
Q
A

Chromophobe Renal Cell Carcinoma

Distinct membranes, large perinuclear halos, vesicles

Colloidal Fe +

137
Q

Dx? associated with?

A

Angiomyelolipoma

associated with Tuberous Sclerosis

usually benign

138
Q
A

Medullary Fibroma

common, benign

139
Q

Baby with this tumor

A

Wilms.

Solid (not renal dysplasia), necrosis

140
Q
A

Blastema: small round cells

Epithelium: tubule formation

Stroma: loose spindle cells

141
Q
A

Wilm’s tumor

primitive glomerular structures (lef)

Blastema

142
Q
A

Blastmea

Epithelium

143
Q
A

ANAPLASIA- bad prognosis

144
Q
A

Urothelial Carcinoma (transitional cell ca)

145
Q
A

Papilloma

benign

146
Q
A

Inverted papilloma

benign

147
Q
A

Low Grade Papillary Urethelial Carcinoma

rarely invades or metastasizes

148
Q
A

High-grade urothelial carcinoma

necrosis, ugly nuclei

149
Q
A

Urothelial CA in situ

Flat red patch grossly

Likely to invade

Positive cytology

150
Q

Country association?

A

Squamous Cell Carcinoma

schistomiasis

EGYPT!!!

151
Q
A

Hyperacute Rejection:

pre-formed antibodies

Thrombosis of vessels -> necrosis

152
Q
A

Acute Rejection:

Tubulitis

(Vasculitis)

153
Q
A

Chronic Rejection

Fibrosis

Thick vessels

Transplant Glomerulopathy: (lamina rara interna thickening)

154
Q

2 most common causes of this

A

Diabetes

Hypertension

155
Q

What is the basic mechanism of Hyaline Arteriosclerosis in hypertension?

A

Endothelial cell damage

156
Q

If you don’t form ONE kidney - prognosis?

BOTH?

A

Unilateral kidney agenesis- okay

Bilateral- stillborn

157
Q

Small, shrunken kidney. How can you tell if its congenital or acquired?

Prognosis?

A

Count the papillae… < 6 = hypoplasia

Unilateral is good prognosis
Bilateral -> renal failure

158
Q

Common location of ectopic kidney?

A

Pelvis

159
Q

Horshoe kidney: prognosis?

A

No

160
Q

Double ureter: problem?

A

Meh. no.

161
Q

Cystic abdominal mass in newborn?

A

Renal Dysplasia

fairly common

unilateral: good prog
bilateral: renal failure

162
Q

Key histological feature of Cystic Renal Dysplasia?

A

Cartilage!

163
Q

AD-PKD:

demographics

Bilateral or unilateral?

Complications?

Location?

A

Common; in adults

Large cysts

***Bilateral!!!!! (if unilateral, think Cystic Neoplasm)

Associated with Berry Aneurysms!

Everywhere

164
Q

AR-PDK

Demographics?

Complication?

Location?

A

Rare, in CHILDREN

Always Bilateral; small cysts (Spongiform Kidney)

Liver involvement (congenital hepatic firosis)

@ Collecting Duct ONLY

165
Q

Alport’s Syndrome:

  • presentation
  • genetics
  • Key histological feature on EM
A
  • Hematuria (later proteinuria, nephrotic synd)
    May also have deafness or eye probs
  • XD mutation for Type IV collage
  • Layering of Lamina Densa in BM
166
Q

Thin Basement Membrane Lesion

(Benign Familial Hematuria)

  • Genetics?
  • Prognosis?
A
  • Familial, asymptomatic hematuria
  • Mutation in Type IV collagen (a5)
  • Normal renal function if heterozygous
167
Q

What causes hyperacute rejection?

A

Pre-formed antibodies

Somebody fucked up at the lab

Causes very quick necrosis

168
Q

Most common finding in Acute Rejection?

Diagnosis?

Timeframe?

A

Tubulitis- interstitial inflammation, maybe vasculitis

IF: C4D!

Can occur at ANY TIME

169
Q

Chronic rejection:

Timeframe?

Findings?

A

Years

See fibrosis, thick vessels, thick GBM (transplant glomerulopathy)

170
Q

Transplant Glomerulopathy:

Type of rejection?

What structure is affected?

A

Chronic rejection

Lamina Rara Interna

171
Q

Bladder: Malignant cytology, but no mass- just red lesions. What is it?

Is this bad?

A

Carcinoma in situ

Frequently invades

172
Q

What is the #1 cause of urolithiasis?

A

Dehydration!!!!

173
Q

What’s the most common composition of stones?

What if the stone is hugeeeee?

A

Calcium

Huge stone = staghorn = Magnesium ammonium phosphate

174
Q

Uricemia is associated with what diseases?

A

Gout

Cancer (lymphoma, leukemia)

175
Q

What is it? Cause?

A

Staghorn stone: caused by proteus infection

176
Q

Most common kidney tumor in adults?

Presentation?

A

Renal Cell CA

Big cystic mass

177
Q

Most common renal cancer in kids?

A

Wilm’s

178
Q

Metastatic disease. Where is it likely coming from?

A

Kidney (clear cell carcinoma)

179
Q

What is this? Associated gene mutation?

A

Clear Cell Renal Carcinoma

associated with Von HIppel Lindau

180
Q

Chromophobe Renal Cell Carcinoma:

What are the structures seen in EM?

A

Cytoplasmic Vesicles

181
Q

Kidney tumor. looks like this:

Prognosis? Invason?

A

Sarcomatoid (spindle cell) Renal Cell Carcinoma

Poor prognosis

Invade bone, lungs, veins

182
Q

Renal Cell Carcinomas: paraneoplastic syndromes?

A

HTN

Hypercalcemia

Polycythemia

Hepatic dysfx

183
Q

Oncocytoma vs. Chomophobe RCCa

A

Oncocytoma: scar, granular cells, Colloid Fe stain (-), benign, mitochondria

Chromophobe RCC: halos, Coll. Fe (+), malignant, vescicles

184
Q

Patient with tuberous sclerosis. Find tumor in kidney. What is it most likely?

A

Angiomyolipoma

185
Q

3 Components of Wilms Tumors

A
  1. Blastema (small cells)
  2. Epithelium (forming tubules)
  3. Stroma (loose spindle cells)
186
Q

What is a marker of poor prognosis in Wilms Tumor?

A

Anaplasia

  • large pleimorphic hypechromatic nuclei (3x normal size)
187
Q

How can you tell that this is Wilms Tumor instead of Renal Dysplasia?

A

Wilms tumor is solid

(Renal dysplasia is cystic)

188
Q

1 symptom?

Urinalysis?

A

Urothelial tumor (aka Transitional Cell Ca)

Hematuria with FRESH RBCs (not casts)

189
Q

1 risk factor of Urithelial tumor?

A

SMOKING

Male, elderly

190
Q

Chronic bladder irritation causes what kind of tumor?

A

Squamous cell carcinoma

191
Q
A

papilloma

192
Q
A

Inverted urothelial papilloma

193
Q
A

High Grade Urothelial Carcinoma

papillary & solid architecture

- necrosis (yellow)

frequently invade

194
Q

How can you get Invasive Carcinoma from normal urothelial tissue?

A

Normal –> Carcinoma in situ –> Invasive Carcinoma

OR

Normal –> Low grade CA –> High grade CA –> Invasive CA

195
Q
A

S4M2 (10 decks)

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