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Year2 Renal > Exam 2 Glomerulonephropathys > Flashcards

Exam 2 Glomerulonephropathys Flashcards

1
Q

where is the renal angle anatomically

A

lower border 12th rib and lateral border of erector spine muscle

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2
Q

describe direction of renal colic pain

A

from renal angle and goes down forward to groin

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3
Q

what components of the kidney are affected by disease

A

glomeruli, tubules, interstitium and blood vessels

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4
Q

what component of kidneys is mostly harmed by immune mediated processes

A

glomeruli

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5
Q

what area of the kidney is most affected by toxic or infectious agents

A

tubules

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6
Q

What is azotemia

A

elevation of BUN and creatinine, decreased GFR

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7
Q

what is pre-renal azotemia? causes?

post renal?

A

pre is hypoperfusion of the kidneys: shock, hemorrhage, volume depletion, CHF
post is obstructed urine flow in distal calyces and pelvis

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8
Q

what is uremia

A

azotemia and a constellation of clinical signs and symptoms

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9
Q

What GFR level is indicative of uremia

A

<20

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10
Q

What are common imaging techniques of the kidney and associated GU organs

A

KUB- plain abdominal film
renal tomography
IVP
retrograde pyelography

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11
Q

what imaging techniques are used to evaluate ureter, bladder and urethra

A

cystography and voiding cytourethrography

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12
Q

how does Nephrotic syndrome lead to edema

A

proteins leaking out of plasma so lose oncotic pressure pull and fluid follows

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13
Q

What are your main Ddx for edema

A

kdiney disease, heart(CHF), liver(decreased production of proteins), GI tract (protein losing enteropathies), Lungs

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14
Q

do plasma proteins have neg or + charge

A

negative so move towards postive pol in electropheresis

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15
Q

Do we regularly do renal biopsies,

A

no because extremely hard to get to. retroperitoneal.

not worth risk

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16
Q

say on a serum strip patient has alot of IgG and Igkappa but not much else

A

multiple myeloma

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17
Q

What are signs of a nephritic syndrome

A

grossly visible hematuria, mild to moderate proteinuria, HTN

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18
Q

What is RPGN

A

rapidly progressive glomerulonephritis with a rapid decline in GFR (hours to days)

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19
Q

what are signs of Acute Kidney injury

A

rapid decline in GFR
oliguria or anuria
can result from glomerular, interstitial, vascular or acute tubular injury
can be reversible

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20
Q

what are signs of chronic kidney disease

A 
milder-really not noticeable
severe- uremia
diminished GFR <60 ml/min for at least 3 months
persistent albuminemia
generally irreversible
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21
Q

What is criteria for ESRD

A

GFR <5% of normal

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22
Q

What syndromes are characteristic of glomerular disease

A

nephritic, nephrotic, asymptomatic hematuria or proteinuria, chronic renal failure, acute renal failure, renal tubular defects

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23
Q

what syndromes are characteristic of tubulointerstitial disease

A

nephrolithiasis, renal tumor, UTI, urinary tract obstrcution, renal tubular defects, acute renal failure

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24
Q

what is criteria for proteinuria in nephrotic syndrome

A

> 3.5 g/day

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25
Q

What are signs of nephrotic syndrome

A

heavy proteinuria >3.5, hypoalbuminemia <3g/dL, severe generalized edema, hyperlipidemia, lipiduria

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26
Q

what occurs to RAAS system with edema from proteinuria

A

activates renin release, so down path causes vasoconstriction of the afferent to kidney which just causes more problems.

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27
Q

selective proteinuria means what

A

albumin and transferrin, low MW proteins

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28
Q

what disease is pure nephrotic syndrome

A

minimal change disease

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29
Q

Why is hyperlipidemia assoc with nephrotic syndrome

A

the liver is trying to increase circulating proteins

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30
Q

why is thrombosis a risk with nephrotic syndrome

A

because may be losing endogenous anticoagulats

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31
Q

what are the systemic causes of nephrotic syndrome

A

DM, amyloidosis and SLE

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32
Q

what primary glomerular lesions lead to nephrotic syndrome

A

minimal change disease, membranous glomerulopathy, and focal segmental glomerulosclerosis

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33
Q

what is the renal corpuscle

A

glomerulus and bowmans capsule

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34
Q

what type of epithelium surround urinary space

A

squamous epithelium

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35
Q

acute kidney injury usually occurs where in the kidney

A

proximal tubules

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36
Q

What is criteria for chronic kidney disease

A

GFR<25%

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37
Q

where is the mesagium in the kidney

A

at the axis of the glomerulus

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38
Q

What are the layers of the glomerulus

A

capillaries have fenestrated endothelium then the BM has lamina rara interna , lamina densa, lamina rare externs then there is the visceral epithelium (podocytes)

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39
Q

What does the PAS stain on glomerulus

A

glycoproteins

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40
Q

What is the role of mesangial cells

A

contractile, phagocytic, proliferate and lay down matrix/collagen, also able to secrete some mediators

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41
Q

What is filtered easily in glomerulus

A

water and small solutes

proteins less than 3.6 nm

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42
Q

what is the barrier to proteins

A

the negative charge in BM repels proteins

also size of filtration slits

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43
Q

What are the slit diaphragm proteins

A

nephrin and podocin with actin cytoskeleton

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44
Q

What could cause the appearance of hypercellularity in the glomerulus

A

cellular proliferation, leukocyte infiltration, crescent formation

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45
Q

What are the 3 forms of BM thickening

A
  1. amorphous deposits like IC on either side, fibrin or amyloid, cryoglobulins etc
  2. increased syntehsis BM proteins (DM)
  3. additional BM in subendothelial locations
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46
Q

Hyalinosis is characteristic of what disease

A

focal segmental glomerulosclerosis FSGS

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47
Q

What is Sclerosis

A

extracellular collagenouse matrix ECM that builds up in mesangium (usually involves capillary loops)
results in fibrous adhesions

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48
Q

What is diffuse sclerosis

A

all glomeruli are affected

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49
Q

what is focal sclerosis

A

only some glomeruli are affected

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50
Q

what is segmental sclerosis

A

only parts of glomeruli are affected

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51
Q

What are the fixed intrinsic tissue Ag that cause Ab-mediated injury in glomerulus

A

NC1 domain of collagen IV Ag
Heymann Ag “megalin” which is a phospholipase A2R
msangial Ag like IgA nephropathy

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52
Q

What is Goodpasture syndrome caused by

A

anti GBM Ab cross react with lungs and kidney BM

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53
Q

what is the histo of goodpastures

A

linear pattern on IF

crescenteric glomerular damage

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54
Q

What does the histo of membranous glomerulopathy look like

A

subepithelial granular pattern on IF

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55
Q

What are the endogenous planted Ag that can lead to Ab mediated glomerular injury

A

DNA< nuclear proteins, Ig, IC and IgA

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56
Q

what are the exogenous planted Ag that can lead to Ab mediated glomerular injury

A

infectious agents and drugs, bacterial products

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57
Q

What is the staining pattern of planted Ag in glomerulopathy

A

granular

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58
Q

What can cause endogenous deposition of premade IC

A

DNA(SLE), tumor Ag

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59
Q

what can cause exogenous deposition of premade IC

A

infectious products, strep, hep B, C

Treponema pallidum, plasmodium falciparum

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60
Q

describe IC deposition based on IC charge

A

anionic will deposit subendothelial b/c can;t cross BM

cationic will cross and make it to the sub epithelial space

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61
Q

where is the subepithelial region

A

between outer GBM and podocytes

“humps”

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62
Q

subepithelial humps are characterisitic of what disease

A

acute glomerulonephritis

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63
Q

epimembranous deposits are characteristic of what diseases

A

membranous nephropathym, heymann glomerulonephritis

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64
Q

subendothelial deposits are characteristic of what diseases

A

SLE nephritis

membranoproliferative glomerulonephritis

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65
Q

mesangial deposits are characteristic of what disease

A

IgA nephropathy

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66
Q

what is unstoppable once GFR is 50% normal rate

A

steady rate of progression to ESRF

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67
Q

What is an example of a complement glomerulonephropathy

A

MPGN type II, dense deposit disease

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68
Q

What is the most common nephropathy worldwide

A

IgA nephropathy

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69
Q

Which type of deposit causes the spike and dome pattern

A

epimembranous

so membranous glomerulonephropathy

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70
Q

What usually is culprit of acute proliferative glomerulonephritis

A

group A beta hemolytic strep

71
Q

what are the morphologicaly changes assoc with acute proliferative GN

A

marked hypercellularity, leukocyte infiltration, subpeithelial hump of IC
neutrophils in the lumen
granular deposits of IgG IgM and C’3 in the masangium

72
Q

what is typical presentation of post strep GN

A

age 6-10
after pharyngitis or skin infection
malaise, fever, nausea, oliguria and hematuria 1-2 weeks after recovery from a sore throat
RBC casts, mild proteinuria, periorobital edema and mild/moderate HTN

73
Q

what is adult presentation of post strep GN

A

more atypical and aggressive course

may exhibit sudden HTN or edema, frequently with elevated BUN

74
Q

what is the prognosis of post strep GN in children?

A

95% recover completely with just water an salt restriction

75
Q

what is the prognosis of post strep GN in adults?

A

60% recover with no sequellae

some progress to RPGN or prolonged time to resolution, progress to chronic glomerulonephritis

76
Q

what can cause acute proliferative GN non-strep

A

other bacteria *staph have IgA not IgG**
viral syndromes: Hep B C, mumps, HIV, varicella
sequel to parasitic infection, malaria, toxoplasmosis

77
Q

What are the 3 major types of rapidly progress GN RPGN

A

type I is Anti-GBM Ab
type II is IC deposition
type III is pauci-immune

78
Q

what are examples of anti-GBM Ab diseases that can turn into RPGN

A

renal limited

Good pasture syndrome

79
Q

What are examples of diseases that can lead to RPGN from IC deposition

A

post-strep (acute prolfierative glomerulonephritis)
lupus
henoch-schonlein purpura
IgA nephropathy

80
Q

What are types of Type III RPGN

A

ANCA-associated, idiopathic and granulomatosis with polyangiitis

81
Q

50% of primary renal diseases associated with RPGN have what type pattern

A

type III pauci immune

82
Q

What HLA subtype is associated with goodpastures

A

HLA DRB1

genetic predisposition to autoimmunity

83
Q

What is the main route of Tx for goodpastures

A

plasmapheresis to remove pathogenic circulating Ab is part of effective Tx regimen which includes immunsuppressive therapy

84
Q

What is Tx method for type II RPGN? type III?

A

does not typically respond to plasmapheresis so Tx if focused on underlying disease
same for type III

85
Q

What is ANCA and what is it assoc with

A

antineutrophil cytoplasmic Ab type III RPGN and may have a role in vasculitis

86
Q

What is the main protein in BM that repels albumin

A

heparin glycoprotein

87
Q

What does RPGN look like morphologically

A

cresenteric formation in glomeruli from proliferation of parietal epithelial cells

88
Q

What is the clinical presentation of RPGN

A

hematuria, RBC casts in urine, moderate proteinuria, variable HTN and edema

89
Q

what are signs of goodpastures

A

hemoptysis and pulmonary hemorrhage

90
Q

What are normal protein levels in 24 urine

A

<150 mg

91
Q

What primary glomerulopathies can cause nephrotic syndrome? state whether more common in children or adults

A 
membranous glomerulonephropathy(adults)
minimcal change disease (children!)
focal segmental glomerulosclerosis(adults)
membranoproliferative glomerulonephritis(children=adults)
IgA nephropathy (adults)
92
Q

what percent of nephrotic syndromes in children is due to primary glomerular disease in US

A

95%

93
Q

what percent of nephrotic syndromes in adults is due to primary glomerular disease

A

60%

usuallydue to systemic process

94
Q

What are the systemic diseases that lead to renal disease

A

DM, SLE, amyloidosis, drugs, infections, malignancies, allergic reactions and random hereditary causes

95
Q

what 3 diseases are pure nephrotic syndromes

A

minimal change
membranous glomerulopathy
focal segmental glomerulosclerosis

96
Q

What HLA is postulated to be linked to primary membranous glomerulopathy

A

HLA DQA1 which is assoc with Ab to PLA2R that has interactions with C’ and the MAC complex

97
Q

what are the deposits made of in primary membranous glomerulopathy?
secondary?

A

IgG4

secondary is IC

98
Q

is the proteinuria selective or non in membranous glomerulopathy

A

nonselective

99
Q

What is morphology of membranous glomerulopathy

A

marked diffuse thickening capillary walls without increase in cellularity
5-20 fold increased thickness in BM
spikes and domes from the deposits (sub epithelial)
effaced foot processes

100
Q

What are signs of membranous glomerulopathy

A

Sudden onset nephrotic or nonnephrotic proteinuria with microscopic hematuria and mild HTN
increased serum creatinine and HTN as it progresses

101
Q

What is the prognosis of membranous glomerulopathy

A

60% have persistent proteinuria
40% develop renal insufficiency
10% progress to ESRD

102
Q

What is the most common cause of nephrotic syndrome in children

A

minimal change disease

103
Q

when is the peak incidence for minimal change

A

2-6 yrs old

after respiratory infection or immunization

104
Q

What is Tx for minimal change

A

corticosteroid therapy

105
Q

What type of cancer is minimal change assoc with

A

hodgkin lymphoma or other lymphoreticular disease

106
Q

What are the presenting signs of minimal change

A

massive proteinuria–> edema!
highly selective for albumin
no HTN or hematuria

107
Q

What is the differentiating characteristic of minimal change and membranous glomerulopathy since both have podocyte effacement

A

in minimal change still have normal glomeruli

108
Q

Where do you see lipid accumulation in the kidneys in minimal change

A

proximal tubules

109
Q

What do you see under IF in minimal change disease

A

nothing, there are not dense deposits of anything

glomeruli pretty normal appearing

110
Q

On IF you see granular IgG and C’3 in GBM in the mesagium

primary on Ddx?

A

acute proliferative glomerulonephritis- nephritic

111
Q

on IF you see linear IgG and C’3 with crescenteric formation

primary on Ddx?

A

Goodpastures- nephritic RPGN

112
Q

on IF you see granular IgG and C’3 diffusely

primary on Ddx?

A

membranous glomerulopathy- nephrotic

113
Q

on IF you see focal IgM and C’3

primary on Ddx?

A

focal segmental GS

nephrotic

114
Q

On IF you see IgG + C’3 and C1q and C4

primary on Ddx?

A

MPGN type I

115
Q

On IF you see IgG and C’3 but not C1q or C4
patient has hematuria and renal failure
what do you suspect?

A

MPGN type II

dense deposit

116
Q

What is the most common cause of nephrotic syndrome in US adults

A

primary FSGS

117
Q

what is the demographic distribution of FSGS

A

most common in hispanics and african american

118
Q

What other diseases are assoc with FSGS

A

HIV, heroid addiction, sickle cell and morbid obesity

119
Q

What are the renal complications assoc with HIV FSGS

A

acute renal failure, acute interstitial nephritis, thrombotic microangiopathies, post infectious glomerulonephritis

120
Q

What is the most severe complication of HIV FSGS? describe it morphologically

A

collapsing FSGS
retraction or collapse of entire glomerular tuft
cystic dilation of tubule segments with inflammation and fibrosis
proliferation and hypertrophy of podocytes
can be assoc with the drug pamidronate

121
Q

What genes are assoc with rare FSGS inherited forms

A

NPHS1 css 19q13 encodes nephrin
NPHS2 autosomal recessive css 1q25-31 encodes podocin
autosomal dominant FSGS from alpha gactinin 4 which is a podocyte actin binding protein
TRPC6 mutations in adult onset FSGS causing an increase in intracellular Ca
css 22 mutations in APOL1(protects against trypanosome infections)

122
Q

who have better prognosis with FSGS children or adults

A

children

123
Q

what is the clinical presentation of idiopathic FSGS

A

higher incidence hematuria, reduced GFR and HTN
proteinuria is nonselective
poor response to corticosteroids
significant progression to chronic kidney disease(atleast 50% progress to ESRD in 10 years)

124
Q

what parts of glomerulus are affected in MPGN

A

glomerular proliferation is predominantly mesangial

125
Q

what is clinical presentation of MPGN type I primary

A

children
nephrotic
microscopic hematuria
mild HTN

126
Q

what is prognosis for primary type I MPGN patients

A

50% develop chronic renal failure over a 10 year span

127
Q

describe clinical presentation of secondary MPGN type I

A 
occurs in adults
frequently associated with chronic antigenemia from: infection, autoimmune or neoplasia
occurs with Hep B, C with cryoglobulinemia
SLE, endocarditis
alpha1 trypsin deficiency
HIV
schistosomiasis
malignancies
128
Q

what is clinical presentation of MPGN II

A 
occurs in children
gross hematuria with nephrotic or subnephrotic proteinuria
profound hypocomplementemia
frequent recurrence
no IgG deposition
129
Q

what causes hypocomplementemia in dense deposit disease

A

persistent C3 activation from C3 nephritic factor circulating around

130
Q

where are the deposits seen on IF for type I MPGN

A

subendothelial

131
Q

what type of MPGN I is most common

A

secondary

132
Q

What is the most common cause of glomerulonephritis world wide

A

IgA nephropathy

133
Q

What is Berger disease

A

Renal IgA without systemic disease

134
Q

What is HSP henoch schonlein purpura

A

IgA nephropathy assoc with systemic disease with skin manifestaions and involvemnent of abdominal viscera

135
Q

describe demographics of IgA nephropathy

A

primarily in older children 2nd and 3rd decades
caucasians and asians> african americans
male predominance 2:1
family history +

136
Q

What is the clinical presentation of IgA nephropathy

A

microscopic hematuria with presence of significant infection at certain body sites and recurrence of infection at same site

137
Q

What other diseases are IgA nephropathy assoc with

A

gluten enteropathy and liver disease

138
Q

What is detected in IF of IgA nephropathy

A

IgA deposits, C3 and properdin but not really IgG IgM

139
Q

what percent of patients with IgA nephropathy progress to chronic renal failure

A

15-40%

very slow process

140
Q

what is the demographics of Alport Syndrome

A

ages 5-20
X linked form
male express full syndrome, females carriers with hematuria

141
Q

what are signs of alport syndrome

A

chronic renal failure, hematuria, nerve deafness, various eye disorders
defects in colagen IV

142
Q

What are the genetics behind alport X linked vs autosomal

A

X lnked is on COL4A5

autosomal on COL4A3 or COL4A4

143
Q

describe morphological appearance of alport syndrome

A

frayed GBM so looks like basket weave or frayed

144
Q

what is thte clinical presentation of alports

A

microscopic hematuria, red cell casts in urine
proteinuria sometimes
hearting issues age 5-20

145
Q

What is the most common cause of benign familial hematuria

A

Thin Basement Membrane lesion

146
Q

What mutations are assoc with thin basement membrane lesion

A

mutations in alpha 3 or 4 chains of type IV collagen

147
Q

What is the inheritance pattern of thin basement membrane liesion

A

autosomal

148
Q

What are the most common leading causes to chronic glomerulonephritis

A 
crescenteric is 90%
membranous nephropathy 30-50%
MPGN 50%
IgA nephropathy 30-50%
FSGS 50-80%
149
Q

SLE patients are more likely to present with nephritic or nephrotic syndrome?

A

nephritic

150
Q

What are the deposits in SLE nephritis and what are they composed of

A

IgG and C’ in the subendothelium

151
Q

what type of glomerular pattern is seen with DM

A

nodular glomerular sclerosis “Kimmelstiel Wilson disease”
and hyalinizing sclerosis in arteries
one of leading causes of chronic renal failure in US

152
Q

DM nephropathy patients have increased risk for what renal pattern

A

pyelonephritis and papillary necrosis

153
Q

what is clinical presentation of DM nephropathy

A

microalbuminuria
non nephrotic proteinuria
nephrotic syndrome
ESRD

154
Q

What is presentation of Amyloidosis and stain color?

A

nephrotic syndrome and die of uremia

stain congo red

155
Q

What is presentation of essential mixed cryoglobulinemia

A

systemic deposits of IgG IgM and ICs

cutaneous vasculitis, synovitis, MPGN type I

156
Q

What does Multiple Myeloma present with in kidneys

A

proteinuria or nephrotic syndrome, HTN and progressive azotemia

157
Q

What is physical signs of Henoch Schonlein purpura

A

skin lesions of extensor surfaces of arms lefs, butt and abdomen

158
Q

What age gorup is most affected by henoch sconlein purpura

A

kids ages 3-8

159
Q

What are the 2 major processes that lead to glomerular nephropathy

A

metabolic defect linked to hyperglycemia and advanced glycosylation end products that thicken the GBM and increase mesangial matrix
Hemodynamic effects associated with glomerular hypertrophy contribute to the glomerulosclerosis

160
Q

What would you expect to see on CT of end stage diabetic kidneys

A

they are shrunken

161
Q

which disease has the cahracterization of “wired looped GBM”

A

the subendothelial dense deposits seen with SLE

162
Q

describe morphology of diffuse proliferative lupus nephritis

A

marked increase in cellularity

glomerulus is increased and seems stuffed into Bowmans capsule with decrease in urinary space

163
Q

What are the two types of acute kidney injury

A

ischemic and nephrotoxic

164
Q

what are common causes of ischemic acute kidney injury

A

decreased effective circulating volume like from hypotension and shock
diffuse involvement of intrarenal blood vessels in conditions like malignant HTN, microangiopathies and systemic conditions associated with thrombosis: HUS, TTP or DIC

165
Q

what cause nephrotoxic AKI

A

drugs, metals, toxins

166
Q

What are the less common types of Acute Kidney Injury

A

acute tubulointerstitial nephritis

urinary obstruction

167
Q

Which area of kidney is susceptible to ischemia and why

A

the proximal tubular epithelial cells have high energy requirements

168
Q

what causes the obstruction in ischemic AKI

A

the necrotic tubular epithelial cells are detached and sloughed into tubular lumen causing obstruction

169
Q

What will it look like morphologically after ingestion of ethylene glycol

A

the proximal tubular epithelial injury is widespread with all cells exhibiting swelling and vacuolization

170
Q

What are the phases of acute tubular injury

A

Initiation- 36 hrs oliguria
Maintenance- oliguric crisis with uremia, hyperkalemia
Recovery-large urine volumes, large loss of water Na K, hypokalemia, susceptibility to infection

171
Q

HepC cryglobulinemia is assoc with what glomerulopathy

A

MPGN type I

172
Q

majority of SLE patients present with nephrotic or nephritic syndrome?

A

nephritic

173
Q

bacterial endocarditis is associated with what glomerulopathy

A

acute proliferative glomerulonephritis

174
Q

kimmelstiel-wilson disease is synonymous with what

A

DM glomerulsclerosis

nodular

Year2 Renal (20 decks)

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