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Pathology > Renal > Flashcards

Renal Flashcards

1
Q

Elevation of blood urea nitrogen and creatinine levels with dec GFR

A

Azotemia

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2
Q

Hypoperfusion of kidneys
Dec GFR
No parenchymal damage

A

Prerenal azotemia

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3
Q

Obstruction of urine flow below kidney

Relief of obstruction followed by azotemia

A

Postrenal azotemia

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4
Q

Azotemia with clinical symptoms and biochem abnormalities

A

Uremia

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5
Q 
Glomerular injury 
acute onset of visible hematuria
proteinuria
azotemia
edema 
hypertension
A

Nephritis

Poststreptococcal glomerulonephritis

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6
Q

Heavy proteinuria >3.5g per day, hypoalbuminemia
severe edema
hyperlipidemia
lipiduria

A

Nephrotic syndrome

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7
Q

Crucial to maintenance of glomerular barrier function as diffusion barrier

A

Podocyte

Also synthesize GBM components

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8
Q

transmembrane glycoprotein of the slit diaphragms between adjacent foot processes

A

Nephrin

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9
Q

Maintains selective permeability of filtration barrier along with nephrin

A

Podocin

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10
Q

Systemic and immunologically mediated diseases affecting glomerules

(SLE, Alport, DM, HUS)

A

Secondary glomerular disease

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11
Q

Two forms of antibody assoc injury in glomerulonephritis:

A

1 deposition of soluble circulating antigen-antibody complex in glomerulus
2 antibodies reacting in situ within glomerulus

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12
Q

pathogens that incite GN

A

1 streptococcal
2 Hepatitis B
3 Plasmodium falciparum malaria
4 Spirochetal

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13
Q

Antigen-antibody complex producing injury through activation of complement and recruitment of leukocyte

A

Glomerulonephritis by immune complex

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14
Q

Electron microscopy of GN show immune complexes on (4)

A 
Mesangium 
Subendothelial (bet endothelial and GBM)
Subepithelial (bet outer GBM and podocyte)
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15
Q

Complexes in endothelium and subendothelium elicit

A

Inflammatory reaction from infiltration of leukocyte and proliferation of glomerular cell

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16
Q

Antibodies directed at subepithelial region of glomerulus produce

A

Noninflammatory lesions similar to Heymann nephritis or membranous nephropathy

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17
Q

Antibodies directed fixed antigen in GBM
LINEAR pattern of staining
Conformational change in alpha3 chain of type IV collagen in GBM

A

Anti-glomerular basement membrane Antibody-mediated crescentic Glomerulonephritis

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18
Q

Complication/sequelae of Anti-GBM Antibody-mediated GN with antibodies also cross reacting with basement membrane of lung alveoli

A

Goodpasture syndrome

simultaneous lung and kidney lesions

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19
Q

Immune injury on Glomerulus pathophy

A

Complement activation via classical pathway:
Chemotactic agents C5a for neutrophil and monocyte
Protease release from neutrophils causing GBM degradation
O2 radical generation causing damage
Arachidonic acid metab causing dec GFR

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20
Q

Antibody mediated GN show this type of pattern desposition

A

Granular

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21
Q

Immune complex antibodies cause injury by

A

1 complement activation

2 leukocyte recruitment with mediator release sometimes damaging podocyte

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22
Q

Nephrotic syndrome clinical complex (4)

A

1 massive proteinuria >3.5g/day
2 hypoalbuminemia <3g/dL
3 Generalized edema
4 hyperlipidemia and lipiduria

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23
Q

Hyperlipidemia in nephrotic syndrome is caused by

A

Inc release of lipoproteins in liver or

Loss of lipoprotein synthesis inhibitors

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24
Q

Most common cause of primary glomerular disease nephrotic in children

A

Minimal-change disease 65%

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25
Q

Most common cause of primary glomerular disease nephrotic in adults

A

Focal segmental glomerulosclerosis 35%

Membranous nephropathy 30%

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26
Q

Primary nephrotic renal disease occurs

A

95% in children

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27
Q

In adults, primary nephrotic disease is caused by

A

Renal manifestation of systemic disease 40%

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28
Q

Glomeruli have normal appearance by light microscopy but show uniform diffuse effacement of podocyte foot processes on EM
Common at ages 1-7

A

Minimal change disease

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29
Q

90% of children respond to a short course of corticosteroid therapy

A

MCD

2/3 will have recurrence of proteinuria

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30
Q

FSGS may be secondary attributed to (5)

A 
HIV
Heroin
IgA nephropathy 2 event
Maladaptation to nephron loss
Mutation in cytoskeletal proteins and podocin for integrity of podocyte and variant in apolopoprotein L1 gene APOL1 on chromosome 22
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31
Q

Injury to podocyte as initiating event
First affects some of glomeruli of JM
Lesions occuring in some tufts within a glomerulus and sparing of others
Inc mesangial matrix, obliterated capillary lumina, deposition of hyaline masses and lipid droplets

A

Focal segmental glomerulosclerosis

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32
Q

Collapse of glomerular tuft and podocyte hyperplasia

Poor prognosis

A

Collapsing glomerulopathy

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33
Q

Hematuria
Hypertension
Non selective proteinuria
Poor response to corticosteroid

A

Focal segmental glomerulosclerosis

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34
Q

Subepithelial IgG deposit along GBM
Diffuse thickening of capillary wall
Chronic immune complex GN by antibodies against glomerular Ag.
Without inflammation

A

Membranous nephropathy

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35
Q

Antigen most commonly recognized by causative antibodies in MN

A

Phospholipase A2

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36
Q

Spike and dome pattern

with granular deposits

A

Membranous nephropathy

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37
Q

MN may be caused by inciting events such as (5)

A 
Infection Hep B, syphilis, schistosomiasis, malaria
Malignancy CA of Lung, colon melanoma
SLE
Inorganic salt gold and mercury exposure
Drugs (Penicillamine, captopril, NSAID)
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38
Q

Full blown nephrotic syndrome without antecedent illness
Non-selective proteinuria
Not responsive to corticosteroid
Protein in 60%

A

Membranous nephropathy

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39
Q

Caused by circulating immune complex or planted antigen with in situ complex
Assoc with Hepa B and C antigen, SLE, AV shunt

A

MPGN Type I

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40
Q

Excess compliment activation against C3 convertase or nephritic factor that lead to uncontrolled activation of alternative complement

A

MPGN Type II

Dense deposit disease

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41
Q

MPGN Type II is associated with mutations in gene encoding complent regulatory factor protein

A

factor H

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42
Q

Hypocomplementemia is marked in MPGN Type II due to

A

excessive consumption of C3 and reduced synthesis by liver

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43
Q

Glomeruli with lobular appearance, proliferation of mesangial and endothelial cell and infiltrating leukocytes
GBM thickening

A

MPGN

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44
Q

Tram track or double contour capillary wall

Splitting of GBM

A

MPGN

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45
Q

subendothelial electron dense immune deposit

C3 in irregular pattern

A

Type I MPGN

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46
Q

Irregular, ribbon-like lamina densa and subendothelial space from unknown composition
C3 present in irregular chunky segmental linear foci
Complement dysregulation

A

Dense deposit disease

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47
Q

Poor prognosis recurring in transplant patients

A

MPGN type II

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48
Q

Underlying mechanism of proteinuria from immune and nonimmune causes

A

Podocyte injury

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49
Q

Nephritic syndrome complex

A

1 hematuria
2 oliguria and azotemia
3 hypertension

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50
Q

Glomerular deposition of immune complexes resulting in proliferation and damage to glomerular cells and infiltration of leukocytes esp neutrophils

A

Acute Postinfectious Poststreptococcal Glomerulonephritis

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51
Q

Others pathogens in Postinfectious GN

A 
Pneumococcal
Staph
Mumps
Measles
Varicella
Hep B, C
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52
Q

Inciting agent in Acute Postinfectious GN

A

Group A Beta Hemolytic Strep

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53
Q

Immune complex disease by complement activation of classical pathway
Hypocomplementemia
Granular deposits of IgG and complement on GBM

A

Poststrep GN

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54
Q

Antigen implicated in PSGN

A

Streptococcal exotoxin B (Spe B)

Streptococcal GAPDH

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55
Q

Increased cellularity of glomerular tuft (diffuse)
Infiltrating neutrophils and monocytes
Subendothelial, intramem or subepithelial humps of immune complexes against GBM
Granular deposits of IgG and complement cleared over 2 months

A

APSGN

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56
Q 
Smoky brown gross hematuria
Oliguria/Azotemia
HTN
Low complement
Inc anti-streptolysin O
A

PSGN

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57
Q

Gross hematuria within 1-2d of URTI

Most common cause of recurrent microscopic or gross hematuria

A

IgA Nephropathy

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58
Q

Most common nephritic glomerular disease revealed by renal biopsy

A

Iga Nephropathy

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59
Q

Deposition of IgA in IgA nepropathy occurs in

A

mesangium

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60
Q

Systemic syndrome involving skin, GI, joints and kidneys with IgA deposition in mesangium

A

Henoch-Schonlein Purpura

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61
Q

Abnormality (inc) in IgA production and clearance

Antibodies against abnormally glycosylated IgA depositing in mesangium activating alternative complement pathway

A

IgA Nephropathy

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62
Q

Secondary IgA nephropathy occurs in

A

Celiac disease

Liver disease defective hepatobiliary clearance

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63
Q

Immunoflorescence shows mesangial deposition of IgA with C3 either focal, diffuse or over crescentic

A

IgA nephropathy

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64
Q

IgA Nephropathy dx

A

biopsy

65
Q

Hereditary disorders caused by mutation in genes encoding GBM proteins
Nerve deafness
Lens dislocation, Posterior cataracts, Corneal dystrophy

A

Hereditary nephritis

Alport Syndrome

66
Q

Foam cells with fat and mucopolysaccharide accumulation in interstitial cells
Thin basement membrane of glomeruli
Basketweave appearance of lamina densa

A

Hereditary nephritis

Alport syndrome

67
Q

X linked heterogenous mutation of gene encoding a5 type IV collagen
M>F, Renal failure
Persistent hematuria

A

Hereditary nephritis

Alport syndrome

68
Q 
Immunologically mediated
12% anti-GBM antibody mediated crescentic GN with or without lung involvement
44% immune complex GN with crescent
44% pauciimmune 
Severe glomerulus
A

Rapidly Progressive Glomerulonephritis

69
Q

Linear IgG

C3 on GBM sometimes on alveolar capillary producing hemoptysis and renal failure

A

Goodpasture Syndrome

Anti-GBM Antibody-Mediated Crescentic Glomerulonephritis

70
Q

Tx for goodpasture

A

Plasmapharesis

71
Q

Enlarged pale kidneys with petechial hemorrhage on cortex

Crescents of parietal cell and mac into Bowman’s space

A

Anti-GBM Antibody-Mediated Crescentic GN

72
Q

Lumpy bumpy pattern of staining for IgG/complement but does not respond to plasmapheresis

A

Immune-Complex Mediated Crescentic GN

73
Q

Segmental necrosis and GBM break with crescent formation

Granular pattern of immune complex

A

Immune-Complex Mediated Crescentic Glomerulonephritis

74
Q

Lack of anti-GBM antibodies or immune deposition
+ ANCA in serum
Sometimes part of microscopic polyangiitis, wegener granulomatosis

A

Pauci-immune Crescentic GN

75
Q

Segmental necrosis and GBM break with crescent formation

No deposits

A

Pauciimmune Crescentic GN

76
Q

Nephritic syndrome with rapid loss of renal fxn

A

RPGN

77
Q

severe glomerular injury with necrosis and GBM breaks and proliferation of crescent

A

RPGN

78
Q

Principal causative organism in acute pyelonephritis

A 
Enteric gram neg
E coli - mc
Proteus
Klebsiella
Enterobacter
Pseudomonas
79
Q

Most important and common route of bacterial infection in kidney

A

Ascending LUTI

also hematogenous at times

80
Q

Important cause of ascending infection allowing bacteria to ascend to pelvis

A

vesicoureteral reflux

20-40% in young children bec of congenital defect

81
Q

Open duct at tip of papilla where urine can be propelled up

A

Intrarenal reflux

82
Q

Discrete yellow raised abscess grossly apparent on renal surface
Liquefactive necrosis with abscess within parenchyma
Non affectation of glomeruli but of the rest

A

Acute Pyelonephritis

83
Q

Necrosis of papilla from DM, obstruction and analgesia

ischemic and suppurative of tips of renal pyramid
Gray white necrosis of 2/3 of pyramids
Coagulative necrosis

A

Papillary necrosis

84
Q

Uneven scarring
Scarring involving pelvis of calyxes
Calyceal deformity

A

chronic pyelonephritis

85
Q

Thyroidization with neutrophils
Chronic inflammation
Arteriolosclerosis
Glomerulosclerosis

A

Chronic Pyelonephritis

86
Q

Edema infiltration by mac and lymhpocytes

A

Drug induced nephritis

Methicillin, thiazide, rifampin - interstitial non-necrotizing granuloma with giant cell

NSAIDs- podocyte foot process effacement

87
Q 
Fever
Eosinophilia
Rash
Renal abnormality
15 days after drug intake
A

Drug induced Interstitial nephritis

88
Q

ATI by AKI

A

oliguria (<400mL/day)

89
Q

Proteinaceous cast in distal tubule and duct along with hemoglobin in ischemic ATI

A

Tam-horsfall protein

90
Q

Thickening and sclerosis of arterial wall and renal changes assoc with benign hypertension

A

Arterionephrosclerosis

Hyaline arteriosclerosis

91
Q

Arterionephrosclerosis implicate mutations in

A

apolipoprotein L1 gene as in FSGS

92
Q

Mutation in apolipoprotein L1 confers protection against

A

tyrpanosomal disease

93
Q

Symmetric atrophy
Diffuse fine granularity like grain leather
Hyaline arteriosclerosis
Fibroelastic hyperplasia of media

A

Arterionephrosclerosis

94
Q

BP >200/120

A

Malignant hypertension

95
Q

Malignant hypertension

A

Kidney vessel injury
Inc permeability to proteins, endothelial injury and platelet with fibrinoid necrosis of arterioles and small arteries
PDGF and intimal hyperplasia lead to hyperplastic arteriolosclerosis
Angiotensin II -> vasoconstriction
Inc Aldosterone

96
Q

Pinpoint petechial hemorrhage on cortical surface
Flea-bitten appearance
Fibrinoid necrosis of small vessel
Onion skin appearance (Hyperplastic arteriolosclerosis)

A

Malignant hypertension

97
Q

Malignant hypertension deaths 90% caused by

A

Uremia

98
Q

Widespread thrombosis in microcirculation

Microangiopathic hemolytic anemia, thrombocytopenia, renal failure

A

Thrombotic microangiopathies

99
Q

Cause of thromoangiopathy

A 
Child HUS
Adult HUS
TTP
Drugs
Malignant hypertension scleroderma
100
Q

Thrombotic microangiopathy pathogenesis

A

Endothelial activation (HUS)
Platelet activation and aggregation (TTP)
Small vessel thrombosis

101
Q

75-% of cases following intestinal infection of Shiga toxin producing E coli or Shigella dysenteriae Type I targetting glomerular endothelial cell
Damage leads to thrombosis

A

Thrombotic microangiopathy

102
Q

Acquired defect in proteolytic cleavage of von Willebrand factor due to autoantibody or inherited defect

A

TTP

103
Q

Autoantibodies are directed against this disintegrin and metalloprotease with thrombospondin like motifs in TTP

A

ADAMST 13

autoantibody binding leads to loss of function and inc large vWF multimers

aggregation and thrombosis

104
Q

25% of children with HUS will develop this consequence secondary to scarring after 25 years

A

Renal insufficiency

CNS involvement
TTP>HUS

Kidney
HUS>TTP

105
Q

Progressive chronic renal damage assoc with HTN

Hyaline arteriosclerosis and narrowing of lumina with cortical atrophy

A

Arterionephrosclerosis

106
Q

Severe elevation of BP
Fibrinoid necrosis and hyperplasia of smooth muscle arterioles and artery
Petechial hemorrhage on cortical surface

A

Malignant hypertension

107
Q

Fibrin thrombi in glomeruli and small vessel -> AKI

A

Thrombotic microangiopathy

108
Q

Childhood HUS is caused by endothelial injury from

A

E coli toxin

109
Q

TTP is caused by

A

defect in vWF ADAMST 13 leading to thrombosis

110
Q 
Symmetrically contracted kidney
Diffusely granular scarring of glomeruli
Obliteration of glomeruli 
Marked interstitial fibrosis 
Unable to ascertain origin of injury
A

End stage kidney disease

111
Q

Pathophysiology of hereditary cystic disease

A

defect in ciliacentrosome complex of tubular epithelial cell

112
Q

1-5cm
transluscent gray glistening smooth membrane filled with clear fluid
single layer of cuboidal cell confined to cortex
Smooth contours on xray, avascular

A

Simple cyst

113
Q

Occur in kidneys of dialysis pxs
Both in cortex and medulla
Hematuria

A

Dialysis acquired cyst

114
Q

Defective gene in 85-90% of families in AD PKD

A

PKD1 on ch 16

115
Q

PKD1 encodes

A

complex cell membrane assoc proten Polycystin-1

116
Q

Renal cystic disease is a type of

A

Ciliopathy

bec polycystin is closely linked to primary cilium of tubular cells

117
Q

hairlike organelles projecting into lumina from apical surface serving as mechanosensor of fluid flow

A

Cilia

Polycystin mutation dysregulates mechanosensing

downregulates cell polarity, proliferation and cell to cell adhesion

118
Q

Mutations in 10-20% of cases caused by this gene

Residing on chromosome

Encoding protein

A

PKD2

4

Polycystin2

119
Q

Ca permeable membrane channel expressed in cilia

Similar phenotype but slower rate of progression

A

Polycystin2

120
Q

Large kidneys palpable with mass of cysts arising from nephrons on all levels
Some may develop asymptomatic liver cyst 1/3
Produces symptoms only on 4th decade of life
Intermittent gross hematuria

A

PCK

75% HTN
10-30% Saccular aneurysm of Circle of Willis and SAH

121
Q

Autosomal recessive childhood PKD is from a mutation in

A

PKHD1 gene encoding receptor protein fibrocystin at ch6

122
Q

Numerous small cyst in cortex and medulla
Spongy kidney
Bilateral
Multiple cysts in liver and bile duct prolif

A

AR Childhood PKD

123
Q

Most common form of nephronopthisis

A

Juvenile

Others: infantile, adolescent, medullary cystic

124
Q

Autosomal recessive form of nephronopthisis affects gene

A

NHP1-9

Encode components of cilia

125
Q 
Small contracted kidneys
Small cysts at corticomedullary junction
Chronic tubulointerstitial nephritis 
Polyuria polydypsia
Unexplained chronic renal failure (diff to dx)
A

Nephronopthisis

126
Q

AD inheritance by mutation in genes encoding polycystin1 and 2
10% of renal chronic failure
Very large kidneys with cyst

A

Adult Polycystic Kidney Disease

127
Q

Mutations in gene encoding fibrocystin
Assoc with liver abnormality
Numerous small cyst

A

Autosomal recessive PKD

128
Q

Cause of chronic kidney disease in children
AR
Mutations encoding epithelial cell protein nephrocysti
Contracted kidney with multiple
SMALL cyst

A

Nephronopthisis

129
Q

3 major stones

A

80% calcium oxalate or calcium phosphate
10% magnesium ammonium phosphate
6-9% uric acid or cysteine

130
Q

Factors contributing to stone formation (4)

A

Concentration of solute
Changes in pH
Bacterial infection
Inc urinary concentration of constituents exceeding solubility in urine (most important) supersaturation

131
Q

50% of patients with calcium stone have

A

hypercalciuria but not hypercalcemia

132
Q

50% of said patients with ca stone absorb ca in gut and excrete promptly in urine

A

absorptive hypercalciuria

133
Q

primary renal defect of calcium reabsorption

A

renal hypercalciuria

134
Q

Occurs in persistently alkaline urine from UTI

Proteus vulgaris, staph

A

Magnesium ammonium phosphate

135
Q

Tendency to excrete persistently acidic urine less than 5.5

Leukemia Gout

A

Uric acid stone

136
Q

Genetically determined defect in renal transport protein of AA
Acidic urine

A

Cysteine stone

137
Q

80% unilateral, stones form in

A

Pelves and calyx

bladder

138
Q

Branching structure creating cast on pelvis made up of magnesium phosphate

A

Staghorn calculi

139
Q

Atresia of ureter, valve formation, aberrant renal artery compression, renal ptosis, kinking of ureter

A

Congenital hydronephrosis

140
Q

Calculi, sloughed necrotic papillae

A

Acquired hydronephrosis foreign

141
Q

BPH, Prostate carcinoma, papilloma and carcinoma tumor, malignant disease

A

Proliferative lesion

142
Q

Prostatitis, uretritis, urethritis, retroperitoneal fibrosis

A

Inflammation

143
Q

SC damage with paralysis of bladder

A

Neurogenic

144
Q

Mild and reversible

A

Hydronephrosis from pregnancy

145
Q

Blockage below level of ureters

A

Bilateral hydronephrosis

146
Q

Dilation of pelvic calyx bec of continued filtration

Initial functional disturbance largely tubular manifested by impaired concentrating ability

A

Hydronephrosis

Serious damage occurs after 3 weeks of complete obstruction

3 months in incomplete

147
Q

Tumors of urinary tract are

A

twice as common as RCC

148
Q

benign tumor from intercalated cells

central stellate scar, plethora of mitochondria

A

Oncocytoma

149
Q

80-85% of primary malignant kidney tumors
2-3% of all cancers in adult
6-7th decade M>F

A

Renal Cell Carcinoma

150
Q

RCC risk factors

A

Smoker
HTN
Cadmium exposure
30x in px with dialysis acquired cyst

151
Q

65% most common
Assoc with homozygous loss of VHL TSP
Invades renal vein

A

Clear cell carcinoma

152
Q

CCC of Kidney strongly assoc to

A

von Hippel Lindau

153
Q

AD
Predisposition to hemangioblastoma of cerebellum and retina
Bilateral renal cyst

A

vHL

154
Q

Palpable abdominal mass
Painless hematuria
Dull flank pain

A

Renal cell carcinoma

155
Q

Assoc with increased expression and mutations of MET oncogene
Bilateral, multiple

A

Papillary renal cell

156
Q

Less common, not as clear as other renal cell carcinoma

A

Chromophobe renal cell carcinoma

157
Q

3rd most common organ CA in children

A

Wilms tumor

158
Q

Cells and tissue components of the tumor in Wilms are derived from

A

mesoderm

epithelial
serosa
blastema

Pathology (24 decks)

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