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CRRAB II- FINAL > Renal Pathology- Warren > Flashcards

Renal Pathology- Warren Flashcards

1
Q

What nephrotoxic cause of ATN will you see oxalate crystals?

A

Ethylene Glycol

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2
Q

What are 2 types of ATN?

A

Ischemic

Nephrotoxic

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3
Q

What are causes of nephrotoxic ATN?

A 
Crush injury (myoglobin)
Urate (from tumor lysis syndrome)
Aminoglycosides
Heavy metals
ethylene glycol
Radiocontrast dye
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4
Q

Normal BUN: Cr ratio?

A

15:1

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5
Q

What kind of casts do you see in ATN?

A

Brown, granular casts

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6
Q

What kind of nephritis do NSAIDs, penicillin, and diuretics cause?

A

Acute Interstitial Nephritis (connective tissue between tubules)

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7
Q

What is found in the urine in Acute Interstitial Nephritis?

A

Eosinophils! High yield

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8
Q

Name one pharmacological cause of renal papillary necrosis.

A

Chronic analgesic abuse

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9
Q

What major protein is lost in nephrotic syndrome?

A

Albumin

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10
Q

Why do patients with nephrotic syndrome develop a hypercoaguable state?

A

They lose Antithrombin III

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11
Q

Why do patients with nephrotic syndrome get hyperlipidemia and hypercholesteremia?

A

Liver reacts by throwing excess fat into the blood because the blood gets “thin”

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12
Q

What is the most common cause of nephrotic syndrome in kids?

A

Minimal change disease

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13
Q

What can Minimal change disease be associated with?

A

Hodgkin Lymphoma (massive overproduction of cytokines from Reed Sternberg cells)

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14
Q

What do you lose in MCD?

Why?

A

Foot processes flatten/efface because of cytokine production

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15
Q

What histology hallmark is present in MCD?

A

NORMAL Glomeruli on H&E stain

EFFACEMENT of foot processes on EM

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16
Q

What is the only protein lost in MCD?

A

Albumin

don’t lose immunoglobulin

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17
Q

What holds together lobules of the glomerulus?

A

Mesangial cells!

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18
Q

What is the most common cause of Nephrotic syndrome in Hispanics and African Americans?

A

FSGS: Focal Segmental Glomerular Sclerosis

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19
Q

What can FSGS be associated with?

A

Heroin Use
HIV
Sicke Cell Disease
(or Idiopathic)

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20
Q

What does “segmental” mean in FSGS?

A

Only a single part of the glomerulus will be involved

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21
Q

What does “focal” mean in FSGS?

A

Only some of the glomeruli in the kidney will be involved

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22
Q

FSGS is the progression of what disease if it doesn’t respond to steroids?

A

Minimal Change Disease

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23
Q

Does FSGS respond to steroids?

A

No…progreses to Chronic renal failure

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24
Q

Most common cause of nephrotic syndrome in caucasian adults?

A

Membranous Nephropathy

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25
Q

Causes of Membranous Nephropathy?

A 
Usually Idiopathic
Hepatitis B/C
SLE-->most common cause of death is renal failure!
Solid Tumors
Drugs
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26
Q

Usually patients with SLE don’t present with nephrotic syndrome, but if they do, what is it?

A

Membranous Nephropathy

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27
Q

What is happening in Membranous Nephropathy histologically?

A

Glomerular basement membrane becomes really thick!

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28
Q

Why does the membrane become thick in Membranous Nephropathy?

A

Immune complex deposition

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29
Q

Where is the immune complex deposition in Membranous Nephropathy?

A

Right under the podocytes (epithelial cells)

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30
Q

How do podocytes respond to immune complex deposition?

A

Try to lay down more basement membrane!

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31
Q

What is the EM description of membranous nephropathy?

A

Spike and dome subepithelial deposits

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32
Q

What do you see in Membranoproliferative Glomerulonephritis?

A

Thick capillary membranes on H and E with “tram track appearance” due to Immune complex deposition

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33
Q

What are the 2 types of Membranoproliferative glomerulonephritis based upon?

A

Location of deposits

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34
Q

What are the 2 types of Membranoproliferative glomerulonephritis?

A

I: subendothelial
II: Intramembranous

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35
Q

Why are there neutrophils in nephritic syndrome?

A

Inflammation is driven by immune complexes which activate complement. A byproduct of this is C5a–these attract neutrophils which mediate damage.

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36
Q

What are RBC casts a sign of?

A

glomerular bleeding

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37
Q

What virulence factor of some Group A Beta hemolytic streps increase the changes of PSGN?

A

M protein! This defines nephritogenic strains

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38
Q

When does PSGN usually occur?

A

2-3 weeks post infection

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39
Q

Is PSGN nephritic or nephrotic?

A

Nephritic

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40
Q

What do you see on EM in PSGN?

A

subepithelial humps

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41
Q

What is RPGN histology?

A

Crescents! Made of Fibrin and macrophages –Inflammatory Debris

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42
Q

What disease have positive p-ANCA?

A

Microscopic polyangiitis

Churg Strauss

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43
Q

Most common nephropathy worldwide?

A

IgA nephropathy

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44
Q

Where do IgA complexes like to deposit?

A

Mesangium

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45
Q

What is Alport Syndrome?

A

Inherited Defect in Type IV collagen that results in thinning and splitting of GBM

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46
Q

What is the genetics of Alport Syndrome?

A

X-linked

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47
Q

What does Alport syndrome present as?

A

Isolated hematuria
Sensory hearing loss
Ocular disturbances

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48
Q

How is polycystic kidney disease inherited?

A

Infant from - autosomal recessive

Adult form - autosomal dominant

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49
Q

What are two things associated with the autosomal recessive form of polycystic kidney disease?

A

Congenital hepatic fibrosis

Hepatic cysts

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50
Q

What three things are associated with the autosomal DOMINANT form of polycystic kidney disease? (adult form)

A

BERRY ANEURYSM
hepatic cysts
mitral valve prolapse

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51
Q

What genes are mutated in adult PKD? what do they code for?

A

**autosomal dominant
APKD1 = encodes polycystin 1 = integral membrane protein

APKD2 = encodes polycystin 2 = Ca+ channel

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52
Q

What is medullary cystic kidney disease? (aka medullary sponge kidney)

A

Autosomal dominant

Cysts in the MEDULLARY COLLECTING DUCTS

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53
Q

What is a gross feature that would distinguish PKD from medullary cystic kidney disease?

A

In PKD kidneys appear enlarged

In medullary the kidneys appear shrunken

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54
Q

What are the hallmarks of acute renal failure?

A

Severe decrease in renal function with in days
AZOTEMIA (increased BUN and creatinine)
Oliguira

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55
Q

How do you distinguish pre-renal azotemia and intrarenal azotemia?

A

Pre-renal will have BUN:Cr>15 (more BUN is getting reabsorbed)

Intra-renal will have BUN:Cr

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56
Q

What will you see in acute tubular necrosis?

A

BROWN granular casts
BUN:Cr 2%
Inability to concentrate urine (urine osm

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57
Q

What cancer can minimal change disease be associated with?

A

Hodgkin Lymphoma

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58
Q

Normal glomeruli
Effacement of foot processes on EM
Selective loss of Albumin
Associated w/ Hodgkin’s lymphoma

A

Minimal Change Disease

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59
Q 
Large hypercellular glomeruli
Sub epithelial "humps"
Smokey Urine
Periorbital edema
Normal in children
A

Poststreptococcal glomerulonephritis

60
Q

Describe Type 1 RPGN

A

LINEAR
Anti-bodies to the basement membrane show a LINE on IF

Good pasture syndrome

Presents with hematuria, hemoptysis, in young adult males

61
Q

Describe Type 2 RPGN

A

GRANULAR
Immune complex depsoition

Usually PSGN or diffuse proliferative glomerulnephritis

62
Q

Describe Type 3 RPGN

A 
Negative IF (pauci-immune)
p-ANCA

Wegener granulomatosis, microscopic polyangitiis, Churg-Strauss syndrome

63
Q

What is the antigen in Anti-GBM glomerulonephritis?

A

NC1 - a component of the noncollagenous domain of Type IV collagen

64
Q

What is the antigen in Membranous glomerulonephritis?

A

M-type phospholipase A2 receptor

65
Q

What is a “planted antigen”?

A

Antigen is non-glomerular in origin, but is localized in the kidney

66
Q

What do you see histologically in Acute Poststreptococcal GLomerulonephritis?

A

Hypercellular glomeruli!

67
Q

What does the EM of Acute Poststreptococcal Glomerulonephritis look like?

A

Subepithelial humps like a camel

68
Q

Is Acute poststreptococcal glomerulonephritis nephritic or nephrotic?

69
Q

How would you describe the urine in Poststreptococcal Glomerulonephritis?

A

Smoky urine

70
Q

When you look at a child with poststreptococcal glomerulonephritis, what is one striking thing you can see instantly?

A

Periorbital edema

71
Q

What do you see histologically in Rapidly progressive GN?

A

Crescents!

72
Q

How many of the glomeruli have crescents in Rapidly progressive GN?

73
Q

Describe the immunofluorescence of Type I RPGN.

A

Linear deposits (anti-GBM)

74
Q

Describe the Immunofluorescence of Type II RPGN.

A

Lumpy-bumpy pattern (immune complex mediated)

75
Q

What is present in Type III RPGN?

A

P or C-ANCA

76
Q

Is RPGN nephritic or nephrotic?

A

Nephritic!

77
Q

What is the most common nephrotic syndrome in kids?

A

Minimal Change Disease

78
Q

In what disease do you see uniform, diffuse thickening of capillary walls and on silver stain you see “spikes”?

A

Membranous Glomerulonephropathy

79
Q

on IF, what are the granular deposits along the GBM in Membranous Glomerulonephropathy composed of?

A

IgG and C3

80
Q

What disease has an increased incidence with Hodgkin’s Lymphoma?

A

Minimal Change Disease

81
Q

What can you use to tx Minimal Change Disease?

A

Corticosteroids!

82
Q

What do you see on EM in Minimal Change Disease?

A

Diffuse effacement of foot processes of the visceral epithelial cells (podocytes)

83
Q

FSGS results from genetic abnormalities to what?

A

Nephrin and Podocin proteins

84
Q

What type of FSGS has the worst prognosis?

A

HIV nephropathy

85
Q

What pathological condition is a mix between nephrotic and nephritic syndromes?

A

Membranoproliferative GN

86
Q

What appearance of Membranoproliferative GN do you see on silver stain?

A

“Tram-track” or double contour due to mesangial cell interposition into the GBM!

87
Q

What is the pathogenesis of Type I MPGN?

A

Immune complex deposition with activation of classical and alternative complement pathways

88
Q

What do you see on EM in Type I MPGN?

A

Subendothelial deposits

89
Q

What is another name for Type II MPGN?

Why?

A

Dense Deposit Disease

Lamina densa of the GBM is ribbon-like and extremely electron dense due to deposits of unknown material

90
Q

When do patients usually get Berger Disease?

A

following an upper respiratory, GI, or urinary tract infection

91
Q

What is the triad in Alport Syndrome?

A

Nephritis
Sensorineural hearing loss
Eye disorders

92
Q

What is the genetics behind Alport Syndrome?

A

Autosomal Recessive

X-linked Dominant Inheritance

93
Q

What is the mutation in Alport Syndrome?

A

Alpha 5 chain of Type 4 collagen

94
Q

What GN is most likely to give you chronic GN?

A

Rapidly Progressive GN

95
Q

How would you describe the IF staining for SLE?

A

“Full house” - stains with everything! So lots of immune components present

96
Q

List the Nephritic syndromes we need to know!

A

“MIA DAR” Kinda dumb i know…but since there is an “i” we know they are nephritic

Membranoproliferative GN
IgA nephropathy
Acute Poststreptococcal GN
Diffuse Proliferative GN
Alport Syndrome
Rapidly Progressive GN
97
Q

List the 3 main nephrotic syndromes we need to know!

A

Minimal Change Disease
FSGS
Membranous Nephropathy

98
Q

What are the other 2 general nephrotic syndromes?

A

Amyloidosis

Diabetic Glomerulonephropathy

99
Q

What is the diagnostic lesion on LM for Diabetic GN?

A

Kimmelstiel-Wilson Lesions

100
Q

What do you see under LM for amyloidosis?

What stain?

A

Apple-green birefringence

Congo Red Stain

101
Q

Most common cause of death in SLE patients?

A

Diffuse Proliferative Glomerulonephritis

Lupus Nephritis

102
Q

Describe the pathogenesis of diabetic nephropathy

A
  • high serum glucose leads to noneznymatic glycosylation of the vascular basement membranes
  • Results in arteriolosclerosis, thickened GBM and increased mesangial matrix
103
Q

When would you see Kimmelstiel Wilson nodules?

A

Diabetic Nephropathy

They are hyaline masses at the periphery of the glomerulus

104
Q

What is the most common causes of acute renal failure? (and presents as acute loss of renal function)

A

Acute Tubular Necrosis

105
Q

Describe the pathology of Acute Tubular Necrosis

A
  • Tubular epithelial necrosis (due to ischemia or toxins)
  • Sloughing of tubular cells into the lumen (obstruction leads to increased intratubular pressure and DECREASED GFR)

-Hyaline and granular casts
Interstitial edema and increased lymphocytes

-Toxic ATN may show specific changes (like calcium oxalate crystals in ethylene glycol ingestion)

106
Q

How would you distinguish an acute from chronic nephritis?

A

Acute - many neutrophils and edema

Chronic- fibrosis and atrophy

107
Q

What are you at increased risk for if you have vesicoureteral reflux?

A

pyleonephritis!!!

108
Q

When are the only two times you will really see any damage to the calyces?

A

CHRONIC PYELONEPHRITIS

and anlagesic nephropathy

109
Q

Name 5 risk factors for acute pyelonephritis?

A
  1. indwelling urinary catheter
  2. urinary tract obstruction
  3. Vesicourecteral reflux
  4. Diabetes mellitus
  5. Pregnancy
110
Q

When is onset of acute drug-induced interstitial nephritis after exposure to drug?

A

approx. 15 days

111
Q

Acute Drug-induced interstitial nephritis is a mixture of what two types of hypersensitivities?

A 
Type 1 (IgE mediated) and
Type 4 (delayed or T-cell mediated)
112
Q

Why do you common see interstitial nephritis in multiple myeloma patients?

A

BENCE JONES proteinuria and cast nephropathy

Directly toxic to tubules!!!

Can combine with Tamm-Horsfall to cause obstructions

113
Q

What is nephrosclerosis? Describe its pathogenesis.

A

The renal pathology associated with the sclerosis of renal arterioles and small arteries

  • medial and intimal vessel thickening secondary to variety of factors
  • Hyaline deposition in arterioles due to endothelial injury with extravasation of plasma proteins and increased basement membrane matrix
114
Q

What is malignant nephrosclerosis?

A

Renal disease associated with malignant hypertension

*pathogenesis unclear

115
Q

What would a “flea bitten” appearance on the gross pathology of the kidney indicate?

A

Malignant nephrosclerosis

116
Q

What would you think if you saw and “onion-skin” appearance of a blood vessel?

A

hyperplastic arteriolosclerosis which involves thickening of vessel wall by hyperplasia of smooth muscle

It is a consequence of…
Malignant hypertension!

117
Q

What are two possible causes of hypertension that is not responsive to HTN medications?

A 
Renal Artery stenosis
Fibromuscular Dysplasia (young women)
118
Q

Describe the pathogenesis of HUS/TTP

A
  • endothelial cell injury
  • Denuded endothelium reveals thrombogenic tissues
  • Reduced prostaglanding I2 and NO
  • Platelet activation and aggregation
119
Q

What causes 75% of Typical/Classical HUS?

A

Verocytotoxin producing E. Coli 0157:H7

120
Q

What four things could cause atypical HUS?

A
  1. Antiphospholipid syndrome
  2. Pregnancy
  3. Vascular renal diseases
  4. Drug related
121
Q

What is deficient in familial HUS?

A

Inhertited deficiency of the complement regulatory protein FACTOR H

-Factor H typically protects cells from uncontrolled complement activation

122
Q

What is the defect in idiopathic TTP?

A

Due to an acquired or genetic defect in the protesase that cleaves large von Willebrand multimers

ADAMTS-13

123
Q

What is hydronephrosis? what is it usually caused by?

A

Distention/dilation of renal pelvis and calyces

Usually caused by urinary tract obstruction

Leads to compression and possible atrophy of renal cortex and medulla

124
Q

Which gender is more likely to get urolithiasis? What is the peak ago of onset?

A

Men > women

20-30 years old

125
Q

What are the four main types of stones?

A

Calcium
Ammonium magnesium phosphate (struvite)
Uric Acid
Cystine

126
Q

What causes struvite (ammonium magnesium phosphate) stones?

A

Caused by infection with urease + bugs that hydrolyze urea to ammonia (resulting in alkalinization of urine)

Commonly form staghorn calcuil

127
Q

Which 3 organisms are urease + that can cause struvite stones?

A

Proteus mirabilis
Staph Saprophyticus
Klebsiella

128
Q

What is the most common type of stone?

A

Calcium (80%)

129
Q

Which two types of stones appear radiopaque on x-ray?

A

calcium

Struvite (ammonium magnesium phosphate)

130
Q

Which two types of stones appear radioucent on x-ray and precipitate at low pH?

A

Uric Acid

Cystine

131
Q

Which stones have the coffin lid appearance?

A

Struvite (Ammonium magnesium phosphate)

132
Q

Cystine stones are rare, what usually causes them?

A

Autosomal recessive condition in which cystine-reabsorbing PCT transporter loses function

Causes cystinuria

Cystine is poorly soluble- thus stones form in urine

common in kids

133
Q

What is an angiomyolipoma?

A

Bengin renal tumor composed of vessels, smooth muslce, and fat

Associated with Tuberus Sclerosis

134
Q

What is an oncocytoma?

A

Benign renal epithelial cell tumor

Presents with painless hematuria, flank pain, and abdominal mass

135
Q

What color is an oncocytoma on gross pathology?

A

Mahogany Brown

136
Q

What is most common primary renal malignancy?

A

Renal cell carcinoma

137
Q

What is the most important risk factor for renal cell carcinoma?

A

Tobacco use (2x more incidence in smokers)

and Obestity

138
Q

What is the classic triad for renal cell carcinoma?

A

Hematuria
Palpable mass
Flank pain

(patients rarely present with all 3)

May also see fever, weight loss, or paraneoplastic sydnrome

139
Q

What gene is deleted in renal cell carcinoma?

A

loss of VHL gene on chromosome 3
(von Hippel-Lindau)

Acts as a tumor suppressor gene –> encodes a protein that is part of the ubiquitin ligase complex (which targets proteins for degradation)

Thus specific proteins that increase transcription and promote angiogenesis are not degraded

140
Q

What is Von Hippel Lindau syndrome associated with?

A

Renal cell carcinoma

Autosomal dominant disorder
Associated with inactivation of the VHL gene leading to increased risk of renal cell carcinoma

141
Q

What are the three subtypes of renal cell carcinoma?

A

Clear cell carcinoma (most common)
Papillary carcinoma
Chromophobe carcinoma

142
Q

Where does renal cell carcinoma like to metastasizes to?

A

Lung or bone

“silent” cancer because commonly presents as a metastatic neoplasm!

143
Q

Why do you sometimes see a left sided varicocele in renal cell carcinoma?

A

Invades the renal vein, and can block drainage of testicular vein

Then goes to the IVC and spreads hematogenously

144
Q

Which renal neoplasm commonly causes paraneoplastic syndromes?

A

Renal cell carcinoma

145
Q

What is the most common tumor of the urinary tract system?

A

Transitional cell carcinoma (urothelial carcinoma)

Usually arises in bladder

146
Q

What is the number one risk factor for urothelial carcinoma?

A

Cigarette smoke!

147
Q

Between HUS and TTP, one is more “renal” and one is more “neurological”…which ones?

A

TTP is more Neurological

HUS has more renal involvement

CRRAB II- FINAL (20 decks)

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