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GIR Test 2 > B5.039 - Pathology of Glomerular Disease > Flashcards

B5.039 - Pathology of Glomerular Disease Flashcards

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1
Q

9th leading cause of death in US

A

kidney disease

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2
Q

what causes ESRD in US

A

DM - 38%

HTN - 24%

Glomerulonephritis - 15%

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3
Q

syndrome of diabetic nephropathy

A

persistent albuminuria >300 mg/d

declining GFR

HTN

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4
Q

renal disease risk factors for death

A

DM

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5
Q

risk factors for developing diabetic nephropathy

A

smoking, low GFR, duration of disease

microalbuminuria

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6
Q

what can slow progression of diabetic nephropathy

A

glycemic control and HTN control

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7
Q

diabetic nephropathy pathophysiology

A

hyperfiltration and hyperperfusion (increased glomerular capillary pressure)

mitochondrial defect resulting in increased ROS

AGE products alter GBM and matrix biochem

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8
Q

diabetic nephropathy histo findings

A

glomeruli - GBM thickening, diffuse mesangial expansion, kimmelstiel wilson nodules, hyalin insudative lesions

vasculature - arteriosclerosis, afferent & efferent

tubulointerstitium - interstitial fibrosis and tubular atrophy, thickened tbm, inflammation

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9
Q
A

Diabetic nephropathy

severe mesangial expansion

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10
Q
A

diabetic nephropathy

K - W nodule

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11
Q
A

diabetic nephropathy

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12
Q
A

interstitial fibrosis in diabetic nephropathy

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13
Q
A

thickened tubular basement membranes

diabetic nephropathy

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14
Q
A

thick glomerular basement membrane

diabtetic nephropathy

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15
Q

describe hypertensive kidney disease

A

25% of ESRD

elevated - 120-29/80

stage 1 - 130-39 or 80-89

stage 2 >140 or >90

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16
Q

causes of HTN

A

most are essential aka unknown

some secondary to renal artery stenosis, kindey issues, aldosteronism

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17
Q

chronic HTN

A

benign

mostly asymptomatic

in kidney characterized by microalbuminuria, decline in eGFR

can cause nephrotic syndrome

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18
Q

accelerated HTN

A

malignant, organ damage

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19
Q

histo of benign HTN kidney disease

A

arteriosclerosis-fibrous intimal thickening

afferent arteriolar hyalinosis

interstitial fibrosis and tubular atrophy

glomeruli have wrinkling early on then glomerulosclerosis

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20
Q
A

HTN

intimal thickening

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21
Q
A

HTN intimal thickening

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22
Q
A

hyalinosis of HTN insudate in small arteriole

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23
Q
A

wrinkling of GBM, a sign of chronic ischemia seen in chronic HTN

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24
Q
A

chronic HTN

solidified glomeruli

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25
chronic HTN glomerulosclerosis
26
pathophys of HTN kidney disease
hemodynamic changes medial/intimal thickening of vessels, endothelial injury afferent arteriolar hyalinosis
27
symptoms of accelerated HTN
visual disturbances, headache,stroke, dyspnea hematuria, proteinuria, coombs negative hemolytic anemia, thrombocytopenia
28
pathology of accelerated HTN
vessels show features of **TMA**, intimal edema. mural fibrinoid necrosis, RBC extravasation and fragmentation, thrombosis TMA especially prominent in arteries TMA changes with proliferation superimposed on chronic changes can create exaggerated layered appearance (**onion skinning**) glomeruli - capillary thrombi, endothelial swelling, necrosis
29
artery shows intimal thickening due to edema from acute HTN
30
Edematous intima, fibrinoid material in intima acute HTN
31
onion skin vessel from TMA due to malingnant HTN
32
pathophys of accelerated HTN
injury to microvasculatrue stimulatino of RAA endothelial injury and dysfunction thrombotic microangiopathy
33
what is TMA
microvascular disease associated with microangiopathic hemolytic anemia and thrombocytopenia disease characterized by non inflammatory injurt to small vessels, associated with fibrinoid necrosis, thrombosis, intima/subintimal edema, RBC extravasation and fragmentation
34
etiologies of TMA
HUS aHUS Autoimmune
35
what is HUS
syndrome characterized by hemolytic anemia, thrombocytopenia, uremia associated with Shiga toxin or shiga like toxin 70% are EHEC (O157:H7) conatminated food most common
36
HUS epidemiology
usually children, summer, prodromal bloody diarrhea occasionaly UTI
37
aHUS pathophys and symptoms
abherant activation of the alternative complement pathway **mutation** in factor H a main driver or acquired **autoantibody** to factor H (which inactivates C3 convertase) uremia, thrombocytopenia, hemoltyic anemia
38
what is TTP
syndrome characterized by hemolytic anemia, thrombocytopenia, uremia, **fever, mental status changes** comes from altered levels of activities of a metalloproteinase ADAMTS13 which normally cleaves vWF preventing formation of ultra large multimers
39
TMA could be due to any of the causes intimal expanded, intimal edema, fibrin
40
TMA glomerular capillaries large and distended by thrombi
41
accelerated HTN can give you what
TMA
42
what is nephrotic syndrome
proteinuria \>**3.5 gm/day** hypoalbuminemia edema hyperlipidema
43
nephritis
hematuria, mild mid proteinuria, HTN, increased sCr, active urine sediment
44
how does nephrotic syndrome occur
abnormalities in the glomerular filtration layer
45
systemic diseases that can cause nephrotic syndrome
**DM** amyloidosis, MIDD SLE
46
diseases that primarily affect glomerluli that cause nephrotic syndrome
membranous glomerulopathy minimal change disease FSGS IgAN, MPGN...
47
clinical presentation of amyloidosis
proteinuria, nephrotic syndrome, **cardiac involvement (arrhythmia, HF)**, fatigue, weight loss, peripheral neuropathy, **hepatomegaly**
48
pathology of amyloidosis
diffuse **expansion of mesangium**/capillary loop basement membranes by **waxy deposits**
49
pathogenesis of amyloidosis
glomerular/vascular deposition of amyloid (abnormal protein with **beta pleated sheet** structure) detected by **congo red** stain usually containing clonal immunoglobulin **light chain lambda**
50
most amyloidosis is caused by what
AL Ig light chain usually associaed with myeloma (CRAB)
51
what is familial mediterranean fever
pyrin mutation, chronic inflammatory disease causing amyloidosis (AA protein)
52
AA amyloidosis
associated with chronic inflammatory state ## Footnote **RA** **inflammatory bowel disease** **Familial mediterranean fever**
53
amyloidosis note waxy apperance of thickened GBM
54
amyloid doesnt stain dark these types of stains note mesangial expansion
55
congo red stain with apple green birefringence a charcteristic of amyloid deposition
56
amyloidosis AL type lambda
57
amyloidosis looks like a ball of hair
58
compare and contrast minimal change, FSGS and membranous glomerulopathy epidemiology
minimal change mostly in kids FSGS mostly adults membranous glomerulopathy mostly adults
59
clinical scenario of membranous glomerulopathy
proteinuria, nephrotic syndrome most common in adult males, early 50s onset
60
labs/clinicl features of membranous glomerulopathy
microscopic hematuria serum complement normal natural hx variable, 1/3 sponaneouslt remit
61
pathology of membranous glomerulopathy
diffuse global thickening of GBM, GBM spikes when capillaries cut in cross section; holes or vacuoles when cute tangentially segmental glomerulosclerosis
62
massively swollen proximal tubule membranous glomerulopathy dots of protein resorption droplets, trying to absorb all the protein
63
clinical risk of membranous glomerulopathy
renal vein thrombosis, if you see a super full vein then think of that
64
membranous glomerulopathy note the really thick basement membrane, normal cellularity
65
membranous glomerulopathy note the little circles, thats the antibody/Ag deposition (immune complexes done pick up stain)
66
membranous glomerulopathy note the little holes where the immune complexes are and the spiky reactive BM formation
67
membranous glomerulopathy little holes, reactive BM spikes
68
what pathology is associated with garland, lei pattern stain for **IgG and C3**
membranous glomerulopathy
69
describe EM and IF for membranous glomerulopathy
IgG and C3 staining in garland or lei pattern EM - subepithelial and/or intramembranous electron dense deposits with GBM projections
70
course **granular** deposits of IgG classic for membranous glomerulopathy
71
subepithelial deposits, membranous glomerulopathy
72
pathophys of membranous glomerulopathy
in situ immune complex formation organ specific autoimmune disorder **autoantibody directed againts PLA2R on podocytes** Ag/Ab complexes shed from podocyt to subepithelial GBM
73
causes of secondary membranous GN
drugs - penicillamine, NSAID, gold Infx - HBV, HCV, syphilis **neoplasm - lung, colon** autoimmune - class V SLE, thyroiditis
74
minimal change disease epidemiology
most common cause of nephrotic syndrome in kids may have transient decline in GFR
75
decribe minimal change presentation
podocyte effacement leading to nephrotic syndrome, responsive to steroids usually proteinuria usually albumin
76
light, IF and EM of minimal change
only EM shows something, diffuse foot process effacement
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minimal change podocyte effacement
78
pathology of FSGS
segmental solidification of capillary tufts PAS and silver + **intracapillary foam cells** and swollen podocytes biopsy might be falsley negative
79
EM and IF of FSGS
IF - non specific trapping EM - foot process effacement
80
FSGS
81
FSGS foot process effacement
82
FSGS
83
classification of FSGS
primary - idiopathic viral - HIV, parvo drugs - heroin, IFN alpha, lithium maladaptive structue/fxn response
84
pneumonic for remembering risk factors for FSGS
Risk factors associated with FSGS can be remembered with the mnemonic MOSAIC\*: Minority (African American or Hispanic) Obesity Sickle cell disease AIDS (HIV) / **APOLI1 gene** IV drug abuse (heroin) and Interferon treatment Chronic kidney disease (secondary to congenital absence or surgical removal)
85
morphologic classification of FSGS pathology
collapsing glomerulopathy - HIV, poorer prognosis
86
collapsing glomerulopathy
classically associated with HIV collapsed glomeruli, tubular microcysts, **tubular reticular inclusions**
87
collapsing glomerulopathy (FSGS) HIV associated
88
collapsing glomerulopathy HIV associated
89
response to sytemic IFN collapsing Glomerulopathy

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