Download Nephritic syndrome (kidney pathology) and more Study notes Pathology in PDF only on Docsity!
-The
Kidney
hritic
Sundromet 2
(^) characterized (^) by inflammation
in the^ glomeruli. & clinical^ features :
- (^) Hematuria /RBCs (^) grad all^ costs^ in^ wrine) Proteinuria (with or^ without (^) edemal
Azotemia (elevated levels^
of ureal Hypertension n.
- Post (^) infections GN & (^) A (^) typical
clinical presentation of^
most proliferative types^ of^
GN - Proliferative Lupus
EN ↑ (^) Proliferation of alls within^ the glomeruli , inflammatory leukocytic infiltrate
- te proliferative stinfections GN)[(PSGN) Characterise diffusepoliferatiof
glomerularaa
caused by (^) Immunecomplexes
-^ Exogenous^ - Endogenous I Postinfections GN^ nephritis^ of SLE-
-oststreptococcal
GN1-^ (m(c) ↑ caused by immune (^) complexes containing streptococcal^ Ag^
. & Specific Ab. =>
- Pathogenesis^ I St Alsstreptocodfetoe hemolytic
streptococc
are nephritogenic
- identifyed by typingof^ M & Latest^ period blu^ infectiono Protein of th bacterial^ cell walls onset^
of nephritis^
is compatible with the^ time^ required for the (^) production
of
actibodies is the^ formation^ of^
insue complexes ↑ Elevated^ Streptococcal Ag
. in^ Pd . D & (^) gracular immune^
deposits
in the^ glomeruli & Streptococcal Ag
. Component^ responsible^ for immune uxh
streptococcal pyogenic^ exotoxin
B (SepB)
& "hump-like" deposits
- characteristic^ of^ disease -
interstital edema^ &^ inflammation O
↑ tubules -^ red^ all^ castsO · Immunofluorescencemicroscopyt
&granular deposits
of (^) IgG S G sometimes IgM
-in mesangium galong
GBM. #tectionmicroscopic^ findings^
- bepithelial deposits^ are -^ discrete, amorphous^ , electron-dense deposits. ↑ (^) Appears as^ "humpin , characteristic e
- Mesangia & intramembraneous^ deposits^ may be -clinical
fectures'
(dysmorphic cells^ (RBC)^ in^ arive
Lab
- · Elevation of Artistreptococcal^ Ab- titers ·↓ in (^) semm Conce of Cy & (^) In children-malaise , fever^ ,^ nausea (^) , oliguria Shematuria /smokyvurine) 1-2 weeks
after recovery^ for^ sore
throat - Colour
and mme
Ag
. Common to^ Alveoli^ & GBM^ - triggers
the formation
of these^ autoantibodies.^
& Treatment-Plasmapheresis
[plame (^) exchange)
isP-seases
caused by immune^ complex deposition with
granular deposits^ of
Ab (^) & Complement (^) by immunofluorescence-
- (^) RPGN is^ a^ complication of (^) any of
the immune Complex
nephritides - Postinfections GN Lupus (^) nephritis IgA nephropathy
Plasmopheresis
iii)
Pauci-immune crescentic^ GNT
anti-GBM Ab^ Con)^
immune complexes
toelectable => by immunofluorescence & electron^ microscopy. ↑ most^ ofs
of
this (^) type have^ circulating Antineutrophil^ Cytoplasmic
Ab CANCAs) that^ produce^
a (^) cytoplasmic (C-ANCA)^ (or (^) perinuclear
(P- ANCA)
Staining
Pattern - #This
is a^ Component^ of^
a (^) systemic vasculitis^ such as granulomatosis with (^) polyangitis.^ (Inflemention of^ Blood (^) vessels)
Mostly limited to^ kidney 3hace idiopathic.
- (^) 1/5th have -^ Anti-GBM^ Ab-mediated GN without long involvement . ->
16th have^ - immune-complex
mediated Crescentic GN -
-Morphology+ · gross
↑ (^) Kidney-enlarged 5 Pale- k often
- Petechial^ hemorrhages^ on the^ cortical^ surfaces based on^ cause, glomeruli^
show-focal
(iv) segmental necrosis
scoPYCrescents^ adjacent^
to (^) glomerular segments^ uninvolved
by inflammatory^
(or) proliferative changes^
is the^ feature of
Eminmure
BPGN.
formed
by-Prolifera
ofommcrepithelia
ese
into the^ urinary^ space . · (^) Neutrophiles & (^) lymphocytes may^
be O
R These^ may obliterate the^ urinary^ space s^ Comes the glomerular · (^) Fibri strands^
- Prominent^ blu^ the cellular^ layess in the crescents. & (^) Escape of procoagulant^ factors, fibrin^ 6 Cytokines^ into
Bowman (^) space (^) may contribute to^ crescent^ formation
Imunofluorescence microscopyI · (^) ImmuneComplex-mediated ses-show
granular
immune =>
deposits . · (^) Goodpasture Syndrome - GBM fluorescence for^ Ige
· Panci-immuneCases - little(r) no^ depositions^ ofinmea
