Flashcards in Non-inflammatory Glomerular Disease Deck (20):
4 aspects that define a nephrOTIC syndrome?
Proteinuria (high, >3.5g/24hr) - important.
4 complications of nephrotic syndromes?
Increased incidence of infection.
4 compartments to look at when analyzing a renal biopsy?
What does segmental vs. global refer to when talking about kidney biopsy findings?
Within one glomerulus, how much is affected: segmental = a small amount.
Global = whole glomerulus is involved
What does focal vs. diffuse refer to when describing renal biopsy findings?
Focal is < 50% of glomeruli are affected.
Diffuse is > 50% of glomeruli are affected.
In miminal change disease, where *do* you see the change in renal biopsy?
There will be podocyte foot process effacement visible on EM.
Etiologies of minimal change disease?
primary - unknown
Secondary: NSAIDs, neoplasms (eg. lymphomas)
Treatment / natural history of minimal change disease?
Corticosteroids induce remission in 90-95% of cases.
Then 1/3 never relapse, 1/3 occasionally relapse, and 1/3 frequently relapse.
(often in children, if this is suspected, steroids are given without biopsy to see if that makes it better)
Some parts of some glomeruli have too much PAS-stainable stuff.
There's no inflammation.
This could refer to the histologic findings of what syndrome?
Focal segmental glomerulosclerosis (FSGS)
What does immunofluorescence in focal segmental glomerulosclerosis (FSGS) show?
Some accumulation of IgM and C3... but it's very mild compared to the immune complex-related diseases.
What does EM of FSGS show?
Podocyte foot process effacement.
No electron-dense deposits.
Collapse of capillary loops with accumulation of "hyalin"... (wouldn't worry about this last one too much)
What cell type is particularly unhappy in FSGS?
How does this affect urinalysis of FSGS?
Podocytes seem to be getting injured and dying, which leads to scarring.
Urinalysis of FSGS will show podocytes in urine, and proteinuria do to decreased podocyte function.
Lots of things can injure podocytes, but there might be underlying genetic susceptibility in patients who develop FSGS.
Yeah.. like age, toxins, immune complexes, metabolic factors, HTN...
What does PAS staining of Membranous Glomerulopathy look like?
Thickened GBM with sclerosis and basement membrane spikes.
What does trichrome staining of Membranous Glomerulopathy look like?
Subepithelial proteinaceous deposits.
What does Membranous Glomerulopathy look like in immunofluorescence?
Granular staining for various things... including complement.
Surprisingly, there isn't other evidence of inflammation.
**I should emphasize that Membranous Glomerulopathy has immune complexes without inflammation.**
How will secondary Membranous Glomerulopathy look different from primary Membranous Glomerulopathy on EM?
Primary: only subepithelial electron-dense deposits.
Secondary: deposits in other places, such as mesangium, subendothelial.
Etiologies of Membranous Glomerulopathy?
Primary = idiopathic/unknown.
Secondary... can be due to a lot of things:
-infection (HBV, HCV, malaria, etc.)
-drugs (gold salts, penicillamine)
-rheumatologic diseases (SLE, etc.)
What does the location of the (non-inflammatory...) immune-complexes in Membranous Glomerulopathy suggest about the way the complexes are formed?
Suggests that the complexes are formed in situ after the constituent elements cross the GBM...