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renal pathology Flashcards

1
Q

what is the leading cause of kidney failure

2nd leading cause

A

diabetes and HTN

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2
Q

renal cortex is responsible for

A

all filtration

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3
Q

most disease in kidney is focused in

A

glomeruli

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4
Q

what portion of the kidney is most sensitive to ischemia?

A

cortex

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5
Q

what portion of the medulla is thick ascending limbs, thick and thin descending limbs and collecting ducts?

A

outer

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6
Q

what portion of the medulla is thin limbs of loop of Henle and distal collecting ducts?

A

inner

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7
Q

what effect on permeability of glomerular capillary wall does increasing negative charge have?

A

decrease

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8
Q

are diaphragms present in fenestrated endothelium pores?

A

no

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9
Q

what is the podocyte membran protein found in podocyte slit diaphragms?

A

nephrin

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10
Q

what makes up the glomerulus filtration barrier

A

endothelium,
basement membrane, and layer
of podocyte foot processes.

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11
Q

inflammation of kidney blood vessels seen in which conditions

A

systemic vasculitis,

transplant rejection

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12
Q

what glomerular histologic alteration is more than 3 nuclei/mesangial area
“Endocapillary” proliferation: endothelial, mesangial, leukocyte
Visceral epithelial proliferation
Parietal epithelial proliferation (“crescent”)
Leukocytic infiltration

A

hypercellularity

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13
Q

T/F: patients w diabetes have a lot of endocapillary hypercellularity of mesangium

A

false- they have a lot of extracellular matrix material that expands that area

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14
Q

T/F: patients w proliferative glomerulonephritis have hypercellularity w lots of neutrophils and lymphocytes

A

true … kids w post-strep infection also can get this, where they have a cross reactive antigen that deposits w/in the GBM starting an immune process

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15
Q

what glomerular histologic alteration can result from Protein deposits: immune complex, organized deposits (polymers)?

A

mesangium

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16
Q

what indicates severe glomerular injury?
is proliferative lesion, composed of epithelial and/or inflammatory cells, collagen and fibrin, and results in partial filling of Bowman’s space?

A

crescents

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17
Q

what changes can you have in GBM

A

thickening
mesangial cell inerpositioning
heterlogous protein deposition
thinning/splitting

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18
Q

what is term for nuclear fragmentation resulting in necrosis?

A

karyorrhexis

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19
Q

what is glomerular hyalinosis

A

deposition of serum proteins

homogenous eosinophilic appearance

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20
Q

global glomerular lesions affect

A

entirety of individual glomeruli

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21
Q

segmental glomerular lesions affects

A

portion of individual glomeruli

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22
Q

diffuse glomerular lesions affects

A

all glomeruli

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23
Q

focal glomerular lesions affects

A

some but not all

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24
Q

3 phases of immune complex disease

A

complex formation
deposition of tissues
activation of inflammatory response

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25
Q

anti GBM disease antibodies directed against

A

type 4 collagen

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26
Q

IF of anti GBM disease

A

linear deposition of Ig along GBM

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27
Q

goodpastures syndrome has

A

anti GBM antibody
renal disease
pulmonary disease

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28
Q

subepithelial deposits fo GBM are associated with

A

“humps” near the outer GBM… these can make it hard to see foot processes

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29
Q

how do immune complexes activate neutrophils and macrophages

A 
by by cross-linking Fc receptors: induces mediator release
Proinflammatory cytokines
Prostaglandins
Chemotactic molecules
Lysosomal proteases
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30
Q

what complex involved in complement cascade via C1 complex consists of C5-9 (cell lysis)?

A

MAC (membrane attack complex)

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31
Q

what components of the complement cascade are Anaphylatoxins that cause vascular permeability?

A

C3a

C5a

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32
Q

what component of the complement cascasde is a Chemotactic products leukocyte migration?

A

C5a

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33
Q

in diabetes, what hormone can cause Glomerular hyperfiltration, which can lead to Glomerular Hypertension, and Hypertrophy of GBM?

A

ANP (atrial natriuretic peptide)

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34
Q

when do you get non-immunologic compensatory hyperfiltration injury?

A
  • occurs when 50-70% nephron mass lost
  • endothelial and epithelial injury of glomeruli
  • glomeruli capillary hypertension
    all these problems lead to focal segmental GS and proteinuria
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35
Q

what is alports syndrome

A

Thinning, splitting, and basket weaving of glomerular BM b/c cant form type 4 collagen\
Also go deaf

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36
Q

if you damage glomeruli you also damage

A

tubules

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37
Q

clinical signs of acute glomerulonephritis

A
  • Hematuria (blood in urine),
  • hypertension
  • Azotemia (increased BUN & nitrate products in body)
  • oliguria (not peeing as much)
  • edema, proteinuria - variable
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38
Q

etiologies of acute glomerulonephritis

A
  • post infectious GN (post-strep)
  • primary glomerular disease -> IgA nephropathy, MPGN
  • multi system diseases -> lupus, vasculitides
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39
Q

rapidly progressing glomerulonephritis will appear clinically as

A

acute nephritis,
rapid progression to ARF

think crescents

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40
Q

pathology of rapidly progressing glomerulonephritis

A

Crescentic Glomerulonephritis-> proliferation of parietal epithelial cells forming a layer >2 cells thick… also will see endocapillary proliferation

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41
Q

pathogenesis of rapidly progressing glomerulonephritis

A
  • there will be severe glomerular, antibody-mediated injury

- can be lupus (most common), also can be IgA, anti-GBM, etc

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42
Q

what defines nephrotic syndrome

A
  • proteinuria > 3.5 g/24 hours (usually they have damage to podocytes which causes this)
  • edema
  • hyperlipidemia, lipiduria
  • hypoalbuminemia (the moment GBM is damaged, albumin gets thru- this tells u kidney is damaged)
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43
Q

pathogenesis of nephrotic syndrome

A

glomerular injury resulting in altered capillary permeability and loss of barrier function w passage of proteins

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44
Q

The moment the GBM is damaged, _______ starts getting thru… this tells u kidney is damaged and can be a sign before the damage gets really bad. Check this in diabetics

A

albumin

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45
Q

what defines nephritic syndrom

A 
hematuria
decreased urine output oliguria
elevated BUN & creatine
HTN
proteinuria, edema
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46
Q

causes of nephritic syndrom

A

Acute post infections glonerulonephritis
IgA nephropathy
Systemic lupus erythematous

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47
Q

proteinuria greater than ____ mg/day is abnormal

A

150mg/day… this could be from a glomerular defect in filtration function of capillary wall, or tubular failure of reabsorption (small proteins usually reabsorbed here)

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48
Q

how do u test for proteinuria

A
  • “dip stick” – detects urine albumin, but not IgL

- Sulfosalicylic acid preparation – detects all proteins

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49
Q

what causes the complication of accelerated atherosclerosis in nephrotic syndrome

A

hyperlipidemia

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50
Q

what is the nephrotic syndrome complication is due to hyperfibrinogenemia & loss of AT III, can lead to Renal vein thrombosis
Pulmonary embolism?

A

hypercoagulation

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51
Q

what type of anemia, due to loss of transferrin, can result as a complication of nephrotic syndrome?

A

hypochronic microcytic

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52
Q

what pathology resulting from a complication of nephrotic syndrome results from loss of Ig?

A

infection

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53
Q

what pathology resulting from a complication of nephrotic syndrome results from loss of cholecalciferol binding protein?

A

hypercalcemia

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54
Q

what pathology resulting from a complication of nephrotic syndrome results from loss of thyroxine binding globulin?

A

hypothyroidism

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55
Q

etiologies of nephrotic syndrome from primary glomerular lesions

A
  • minimal change disease
  • focal segmental glomerulosclerosis
  • membranous glomerulopathy
  • membranoproliferative glomerulopathy (often nephritic)
  • IgA nephropathy (often nephritic)
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56
Q

etiologies of nephrotic syndrome from systemic diseases

A
  • diabetes
  • SLE
  • amyloidosis
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57
Q

what disease accounts for over half of the nephrotic syndrome cases in kids?

A

minimal change disease… peak age is 2-6 yrs old

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58
Q

clinical features of minimal change disease

A

proteinuria highly selective for albumin

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59
Q

how do u detect MCD

A

nothing shows up on light microscopy or IF!

you will see extreme podocyte damage on electron microscopy!!

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60
Q

most kidney problems start with ____________ that pisses off immune system leading to kidney dis

A

upper respiratory infection

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61
Q

clinical features of FSGS (focal segmented glomerulosclerosis)

A
  • proteinuria (may or may not be in nephrotic range)
  • hematuria v common
  • *normal renal function early, but later progressive loss of function (e.g. creatinine begins to rise)
  • hypertension
  • affects both children & adults, M>F
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62
Q

FSGS much higher incidence in

A

african americans

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63
Q

histo of FSGS

A
  • focal, segmental, global glomerulosclerosis
  • segmental sclerosis of any glomeruli is abnormal and indicates glomerular injury
  • global sclerosis of small numbers of glomeruli is normal (when this becomes >10% u have a problem)
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64
Q

FSGS pathogenesis

A
  • decreased renal mass can lead to this
  • morbid obesity- causes kidneys to work harder
  • chronic pyelonephritis - more common in women except in older men when prostate clamps bladder
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65
Q

what is collapsing glomerulopathy

A

Worse variant of FSGS related to HIV or idiopathic. Fastest developing and leading to kidney failure.

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66
Q

clinical signs of collapsing glomerulopathy

A
  • massive proteinuria
  • rapid progression to renal failure
  • poor response to therapy
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67
Q

pathogenesis of membranous glomerulopathy (MGN)

A

immune complex deposition

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68
Q

etiologies of membranous glomerulopathy (MGN)

A
  • autoantibody against glomerular epithelial cell antigens (idiopathic)
  • happens secondary to: malignancy, SLE (called membranous lupus nephritis), and infection
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69
Q

you see spikes and holes in jones silver stain w which dis

A

membranous glomerulopathy (MGN)

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70
Q

clinical presentation of MGN

A
  • nonselective proteinuria, usually nephrotic
  • hematuria common
  • hypertension rare
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71
Q

what do u see on IF of MGN

A

granular IgG and C3 along capillary wall

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72
Q

what kind of deposits are in MGN

A

subepithelial

73
Q

immune complex mediated MPGN is characterized by

A

cellular proliferation and thickening of capillary walls

74
Q

MPGN type I (most common) presentation:

A
  • proteinuria (usually nephrotic, but may be mild)
  • hematuria
  • hypocomplementemia (low serum C3 levels)
75
Q

pathology of glomeruli in type I MPGN

A
  • hypercellularity-> mesangial and infiltrating mononuclear cells in global distribution
  • thick walled capillary loops ->double contour or tram-track appearance of GBM (seen on silver)
76
Q

ultrastructure of MPGN type I

A

electron dense, immune deposits in subendothelial and mesangial locations… new BM material laid down by endothelial cells over deposits & cells

77
Q

IF of type I MPGN

A

granular C3 along the GBM at the periphery of the lobules (w central sparing), mesangial deposits may be present also

78
Q

MPGN type I etiology

A
  • immune complex pathogenesis -> activated by complement

- also can happen secondary to systemic illness: SLE, Hep C

79
Q

what happens in MPGN type II: Dense Deposit Disease

A

Autoimmune dis (aka C3 nephritic factor) directed at C3bBb (C3 convertase). Antibody stabilizes the enzymes, prevents its degradation, leads to increased complement activation and consumption

80
Q

IF of MPGN type II

A

smooth, ribbon-like deposits of C3 along glomerular capillary wall (pseudolinear)

81
Q

clinical course of type 1 MPGN

A

Persistent or intermittent Nephrotic Syndrome
Gradual progression to renal failure (30-50%)
Prognosis worsens with nephrotic proteinuria

82
Q

clinical course of type 2 MPGN

A

Progresses to renal failure in most cases

Frequently recurs in transplanted kidneys

83
Q

diabetic glomerulosclerosis accounts for __% of deaths in pts <40yrs

A

20

84
Q

diabetic glomerulosclerosis histo:

A
  • nodular glomerulosclerosis–> Kimmelstiel-Wilson disease
  • small vessels (arterioles) damaged before arteries in diabetes
  • PAS & silver positive
85
Q

you see nodular glomerulosclerosis on histo in which diseases

A
  • diabetes
  • amyloid
  • light chain
  • MPGN
86
Q

capsular drop/fibrin cap is damage that can occur to bowman’s capsule from

A

diabetes

87
Q

diabetic glomerulosclerosis EM

A
  • diffuse uniform thickening of GBM

- mesangial matrix expansion

88
Q

what are deposition disorders

A

Diverse group of diseases characterized by deposits of protein often in ultrastructurally organized forms

89
Q

immunoglobulin derived deposition disorders

A

amyloidis and cryoglobuinemia

90
Q

what amyloid protein seen in amyloidosis is associated with plasma cell dyscrasias (e.g. multiple myeloma), composed of monoclonal light chain fragments (usually lambda light chains)?

A

AL (primary)

91
Q

what amyloid protein seen in amyloidosis is associated with chronic disease
derived from serum amyloid A protein by proteolytic cleavage and polymerization?

A

AA (secondary)

92
Q

amyloidis presenting features

A

renal disease with proteinuria often nephrotic, reduced renal function, rarely HTN

93
Q

what stains amyloidis

A

congo red

94
Q

what is cryoglobulins

A

serum proteins that precipitate upon cooling

95
Q

cryoglobulinemia associated with

A

HCV hep c

96
Q

cryoglobulinemia associated with

A 
Raynaud’s phenomenon 
Vasculitis 
Arthralgias 
Purpura
Hypocomplementemia: reduced C1, C4, but elevated C3
97
Q

cryoglobulinemia appears

A

usually appears years after systemic onset:
Hematuria in almost all cases
Proteinuria, +/- nephrotic syndrome (20%)
Acute renal failure

98
Q

cryoglobulinemia looks like

A

MPGN
Hypercellular, lobulated glomeruli with “double contours”
Capillary loop ‘pseudothrombi’ (cryoglobulin deposits)

99
Q

whta type of deposits in cryoglobulinemia

A

Large subendothelial deposits composed of distinctive annular or tubular structures

100
Q

types of congenital nephrotic syndromes

A

finnish type
diffuse mesangial sclerosis
congenital syphilis

101
Q

clinical features of acute post-infectious glomerulonephritis

A
  • ** anti strepolysin O
  • acute nephritis -> oliguria, periorbital edema, hypertension, smokey urine
  • decreased C3 (returns to normal w/in 2 wks)
  • pathogenesis occurs 2 wks after infection
102
Q

IF of acute post-infectious glomerulonephritis

A

coarse granular deposits of IgG and C3

103
Q

what is the most common primary glomerulonephritis

A

IgA Nephropathy (Berger’s dis) -
peak age is 15-30 yrs old
M>F

104
Q

presenting feature of IgA nephropathy

A

asymptomatic hematuria … this is usually a very slow progressive dis

105
Q

pathogenesis of IgA nephropathy

A

IgA immune complexes are abnormal, so it cannot be degraded in liver.

106
Q

etiologies of IgA nephropathy

A

Chronic liver disease,
Crohn’s dis,
gluten enteropathy,
chronic bronchitis

107
Q

IF of IgA nephropathy

A

mesangial granular IgA

108
Q

serology of lupus-

A

anti-nuclear Abs, decreased C3

109
Q

when patients w/SLE have anti-phospholipid Abs

A

predisposed to thrombosis (DVT),

predisposed to repeated miscarriages

110
Q

full house staining is seen in

A

SLE

deposits everywhere, subendo and mesangial

111
Q

C1q deposits only really seen in

A

lupus

112
Q

rapidly progressive glomerulonephritis RPGN characterized by

A

rapid loss of renal function (acute renal failure)… typically associated with glomerular crescent formation. Creatinine will skyrocket quickly.

113
Q

IF of anti-GBM dis

A

continuous linear IgG along capillary walls

114
Q

what is ANCA

A

‘anti-neutrophil cytoplasmic antibodies’ are antibodies directed against neutrophil granule contents

115
Q

Wegner granulomatosis usually affects

A

upper/lower respiratory tracts, M>F, age 40

116
Q

Wegner granulomatosis looks like ___

A

anti GBM but they have negative IF not linear

117
Q

prerenal causes of acute kidney failure

A

Due to hypoperfusion (blood isn’t getting to kidney which is causing damage). Often caused by trauma

118
Q

postrenal cause of acute kidney failure

A

urinary tract obstruction

119
Q

intrarenal causes of acute kidney failure

A

due to disease of renal parenchyma:

  • glomerular: RPGN
  • vascular: vasculitis, thrombosis, thrombotic microangiopathies
  • acute tubular necrosis, acute tubulointerstitial nephritis, myeloma cast nephropathy
120
Q

acute tubular necrosis is the most common cause of

A

ARF

121
Q

clinical features of acute tubular necrosis

A

acute decline GFR
oliguria/anuria
rising BUN and creatine

122
Q

what is the major cause of acute tubular necrosis

A

ischemia

- also can be caused by toxicity from antibiotics and radio-contrast agents

123
Q

what makes kidneys susceptible to acute tubular necrosis?

A
  • they receive 25% of cardiac output
  • substances are concentrated in tubules of kidneys
  • have a lot of mitochondria/need a lot of oxygen
124
Q

histo of acute tubular necrosis

A
  • proximal tubular dilation and flattening of epithelium

- granular casts in distal tubules

125
Q

which antibiotics can cause acute tubular necrosis

A

aminoglycosides,

amphotericin B

126
Q

acute tubulointerstitial nephritis clinical features

A

acute renal failure -> increased BUN and creatinine

- symptoms occur 2 wks after drug was started, if stopped can get full recovery

127
Q

what are causative agents of acute tubulointerstitial nephritis

A

antibiotics, diuretics, anticonvulsants, non steroidal and non inflammatory and antacids

128
Q

which antibiotics cause acute tubulointerstitial nephritis

A

penicillins and cephalosporins

129
Q

histo of acute tubulointerstitial nephritis

A

inflammation in interstitium
infiltrating cells: eosinophils!!!
inflammation in tubulues with or without necrosis

130
Q

acute tubulointerstitial nephritis subtypes?

A

analgesic and NSAID nephropathys

131
Q

analgesic nephropathy increased risk for

A

transitional cell carcinoma

132
Q

NSAID nephropathy

A

cyclooxyygenase inhibitors mess w kidney’s ability to maintain BP

133
Q

Myeloma cast nephropathy - clinical features?

A

acute or chronic renal failure,

proteinuria- not detected on dip stick

134
Q

pathology of myeloma cast nephropathy

A

eosinophil casts,
fractured casts- they’re hard as rocks so crack when u cut thru them for staining,
these casts have a 2-toned look- easy to spot,
tubular epithelial damage or necrosis

135
Q

what is unusual about IF of myeloma cast nephropathy

A

Only one light chain isotope shows up- usually kappa, or lambda. In normal patients these would have equal staining

136
Q

vascular diseases of kidney

A 
Benign Nephrosclerosis
Malignant Nephrosclerosis
Systemic Sclerosis
Thrombotic Microangiopathies
Vasculitides
137
Q

what is renal disease in benign HTN

A

benign nephrosclerosis

138
Q

clinical features of benign nephrosclerosis

A

proteinuria and or slow progression to renal failure

139
Q

renal disease in malignant HTN

A

Malignant nephrosclerosis

140
Q

“onion skinning” hyperplastic arteriolosclerosis

A

Malignant nephrosclerosis

141
Q

Malignant nephrosclerosis clinical features

A

renal failure and death if not treated immediately

142
Q

hrombotic microangiopathy is a group of disorders characterized by

A

microthrombosis of arterioles and capillaries, which is caused by microangiopathic hemolytic anemia

reduced platelets
often with ARF

143
Q

hemolytic-uremic syndrome can cause ________________, which can often lead to acute renal failure & death in 1/2 adults who get this

A

thrombotic microangiopathy

144
Q

pathogensis of thrombotic microangiopathy

A

endothelial cell injury
platelet aggregation
together cause vascular obstruction

145
Q

Hemolytic-Uremic syndrome clinical finidings

A

acute renal failure,
thrombocytopenia,
hemolytic anemia

146
Q

types of renal allograft rejections

A

hyperacute
acute
chronic

147
Q

clinical features of hyperacute rejection

A

anuria, fever, pain

immediate kidney removal necessary

148
Q

when does acute rejection cocur

A

few weeks to months

149
Q

clinical features of acute rejection

A

sudden azotemia(elevated creatine/BUN)
oliguria
sometimes fever, graft tenderness

150
Q

pathology of acute cellular rejection to kidney transplant

A

interstitial inflammation: lymphocytes (T cells) come in & damage organ

151
Q

clinical features of chronic rejection

A

progressive azotemia, oliguria, HTN months to years after

152
Q

chronic rejection of kidney transplant - pathology?

A
  • intimal sclerosis/proliferation of small and large arteries, may be obliterative
  • not responsive to therapy
153
Q

primary diseases most likely to reccur after kidney transplant?

A

Membranoproliferative glomerulonephritis
Anti-GBM disease
IgA nephropathy
Focal segmental sclerosis, variable

154
Q

why is urinary tract obstruction important to detect?

A
  • it’s usually easily correctible,
  • often affects young children,
  • results in irreversible renal damage & ultimately failure if untreate
155
Q

causes of urinary tract obstruction

A

benign prostatic hypertrophy,
tumors,
calculi (stones,
congenital abnormalities in kids

156
Q

what is hydronephrosis of urinary tract

A

dilation of renal pelvis, calyces and ureter due to obstruction

157
Q

what is hydronephrosis of urinary tract obstruction associated with

A

atrophy of kidney and blunted papillae

158
Q

microscopic features that characterize acute urinary tract obstruction-

A

dilation of tubules & bowman’s space

159
Q

__________ = formation of stones within urinary tract

A

urolithiasis

160
Q

clinical features of urolithiasis depend on

A

stone size

161
Q

small stones of urolithiasis would cause

A

severe pain if enter the ureter, due to obstruction

162
Q

large stones of urolithiasis would…

A

stay in renal pelvis & are asymptomatic

163
Q

types of urolithiasis

A

calcium
struvite
uric acid
miscellaneous-cystine

164
Q

which type of urolithiasis forms after infection with urea-splitting bacteria (proteus mainly)?

A

struvite

165
Q

which urolithiasis can result in large “staghorn calculi”

A

struvite (magnesium ammonium phosphate)

166
Q

which type of urolithiasis is most common?

A

calcium (oxalate & phosphate)… often associated w increased calcium excretion

167
Q

benign renal tumors

A

oncocytoma
angiomyolipoma
papillary adenoma

168
Q

malignant renal tumors

A

renal cell carcinoma
wilm’s tumor
urothelial carcinoma

169
Q

most common cause of renal cell carcinoma?

A

most are sporadic!

170
Q

renal cell carcinoma is autosomal __

A

dominant

171
Q

clinical features of renal cell carcinoma

A

hematuria
costovertebral pain
palpable mass
fever, malaise, weakness, weight loss

172
Q

classification of renal cell carcinoma based on

A

histology, cytogentics, genetics

173
Q

clear cell carcinoma most commonly affect

A

upper pole of kidney

174
Q

most common type of renal cell carcinoma

A

clear cell carcinoma

175
Q

clear cell carcinoma have abundant clear cytoplasm with

A

accumulation of lipid and glycogen

176
Q

what is the most common primary renal tumor of children

A

wilms tumor

177
Q

wilms tumor has germline mutation in

A

WT1

178
Q

clinical features of wilms tumor

A 
large abdominal mass
hematuria
pain
intestinal obstruction
HTN

pathology (8 decks)

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