glomerulonephritis Flashcards
different causes of GN
- infection - post strep
- autoimmune - ra, lupus abitglomeular bm disease
- deposition - amyloid
- metabolic - diabetes
- malignancy
- drugs- nsaids, anabolic steroids
- Hereditary disorders e.g. Alport’s syndrome
what does selective mean
only albumins
what is proliferative GN MORE associated with but not a rule
nephritic
difference between iGA AND PSGN
both after an URTI but IG A will have 1 or 3 day history whereas PSGI is > 1 week ( I think) may have even recoverdd
what is the ubiquitous feature of FGS
proteinuria which may be nephrotic or non nephrotic
FGCS - what happens to podocyes
atrophy
MCD- hat happens to podocyes
effacement
secondary causes of membranous GN
malaria, hep b , lupus
membranous gn has a high risk of
clots especially in renal vein
typically what’s the progression form pharyngitis to kidney problems in PSGN
around 10 days
‘synpharyngitic syndrome’
in psgn Short latency period <1 week is suggestive of ‘synpharyngitic syndrome’
corresponding typically to exacerbation of underlying IgA nephropathy
what type pf hematuria is present in PSGN
Microscopic in more than two-thirds of cases but can be macroscopic sometimes
classification of hypertension in PSGN
mild to moderate and typically goes away after diuresis
main staining pf PSGN
C3( always ) AND IG G (varying in intensity ) but in talas table they come together
ubiquitous MCD
MASSIVE PROTEINURIA
PATHOGENEISS OF MCD
T cells in the blood release cytokines which damage the foot
process of the podocytes (effacement) This leads to selective
proteinuria
Type of staining in membranous
Granular subepithelial immmune complexes of c3 and IG G
Kidney function in membranous
Normal and slightly decreased
The difference between primary and secondary memrbnois
1- antibodies attacking the podocytes (antiphospholase A2 receptor)
No mesanagium
iG G subclass 4
Secondary
Competes deposited
Mesangium
Subclasss 1,2,3
What type of proteinuria is membranous
Non selective
Membranoprolofeative usually affects
Children
Type 1 and type 2 membrano proliferative
- Subendothelial + mesangial proliferation
Type 2 : intramembranous- DDD + mesangium
Type 3: subepi, subendo, mesangium
Which types of membranoprolifertive have hypocomplimentemia
Both
Which GN have low complement
PSGN and membranoproliferative
Where is c3 nephrotic factor found
In type 2 membranoproliferative but also can be found in type 1
Where is terminal complement nephrotic factor found
Mainly in type 3! But can be found in type 1 too and rarely in type 2
DDD
membranoproliferazive type 2(intramembranous)
subepthelial hum like despots of IG G and c3 is
PSGN
ig m neproptahthy
you’ll have regular staining which is dominant in the mesangial area
ELECTRON DENSE DEPOSITS (dx with MCD)
which one has irregular staining for iG m
FSGS
Whas the pathophys for crescent formation
Hypergonadotropic hypogonadism indicates a primary gonadal defect (congenital or acquired), while hypogonadotropic hypogonadism suggests a hypothalamic/pituitary process (congenital or acquired)
classification of crescneetirc
Classification of crescentic GN based on IF and serologic criteria
Type 1 –linear deposits of IgG - anti glomerular basement membrane disease
Type 2 –granular deposits of immunoglobulin – immune complex mediated
Type 3 – few/no immune deposits (pauci – immune) – anti neutrophil cytoplasmic
antibody associated (ANCA associated) – related to small vessel vasculitis! such as weighers granulomatosis
Type 4 – combinations of type 1 and 3
Type 5 – ANCA– negative pauci immune renal vasculitis – 5-10%
antiglomerular bM what type of staining
LINEAR
where do we find the antiphosopholipase receptor
primary membranous GN
