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S&D 3
Block 4
11. Renal Pathology D - Cox
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Created by
Jean Taleangdee
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Cards (19)
diabetic kidney disease - longstanding
hyperglycemia
will cause
mesangial matrix expansion
thickening
pattern
lesion due to
deposition
of
lipohyaline
What is the primary driver of damage in DKD?
hyperglycemia
DKD - hyperglycemia will cause
formation of
glycation end production
activated
immune destruction
excess ECM = increase type
4 collage
+
degradation
by
MMP
hyperglycemia
will cause
podocyte damage
leading to destruction of GBM
resulting in
segmental glomerulosclerosis
DKD - matrix expansion: nodular is called
Kimmelstiel Wilson lesion
DKA - there is
tubular atrophy
due to
chronic interstitial inflammation
leading to
papillary necrosis
DKD - There is
diffuse thickening
of
GBM
(early
structural
change)
mesangial region expanded
due to
increase mesangial matrix
hyalinosis
lesion
foot process effacement
and
podocyte loss
DKA clinical
persistent microalbuminuria 30
-
300
progress to
macroalbuminuria
>
300
mg/d
leading to
end stage renal disease
elevated
arterial BP
amyloidosis
-
insoluble
protein -
beta pleated sheets
- deposited in
organs
Amyloidosis deposits in
glomeruli
tubulointerstitium
tubules
(amyloid casts)
vessel walls
amyloidosis
will make the kidney
larger
due to
deposition
and
mass effect
systemic
lupus
erythematosus associated
immune
complex mediated
renal
injury
activate
classical complement pathway
leading to
inflammation
Lupus - Full House:
IgG
,
IgA
,
IgM
,
C3
,
C1q
positive
Lupus:
tubuloreticular
inclusion - use for establishing
diagnosis
reticular aggregates in
endothelial
cells
What can you find in RPGN?
glomerular crescents
RPGN pathology to crescents
endothelial injury
rupture of
GBM
trigger
coagulation cascade
within
bowman's space
fibrin deposition
stimulation of
parietal
epithelial
cell
proliferation
RPGN -
crescent
will lead to collapse
glomerular
tuft and
tubular
outflow
obstruction
RPGN -
flea
beaten appearance due to
petechial hemorrhage
RPGN - rapid renal dysfunction
will have
Acute nephritic
syndrome