Focal Segmental Glomerular Sclerosis(FSOS) Flashcards
how many patient might go to CKD
2/3rd people
becoz
Decrease in Podocytes
Synechiae lead to sclerosis
Two type of FSGS
Primary
secondary
Secondary FSGS is
Nephrotic range protenuria
Elderly HTN
LM- FSGS
IF-Normal
EM-Podocyte effacement<50%
Causes of secondary FSGS
Drugs
IF-alpha
Pamidronate
Sirolimus
Heroin
Infections
Parvo B19
HIV
Genetics
Autosomal recessive
Autosomal dominant
Adaptive FSGS or Peri hilar FSGS
Hyperfiltration injury
(Reflux, RAS)
Miscellaneous
Obesity
Anabolic steroids
Cyanotic congenital heart disease
Hyperfiltration injury the opposite kidney undergoes is called
Adaptive focal segmental glomerular sclerosis
Secondary FSGS presents with
Nephrotic protenuria without syndrome
IF–ve
Podocytes effacement<50%
Primary FSGS is due to
Circulating permeability factor
SUPAR(soluble urokinase plasminogen activator receptor)
Presentation of primary FSGS
75% nephrotic syndrome
25% asymptomatic micro hematuria protenuria (better prognosis)
Primary FSGS
Classical IF- focal IGM+- C3
EM-
50% effaced
What is tip variant FSHS
Best prognosis
Behaves like MCD
Collapsing variant FSGS
Worst prognosis
HIV
heroin
Pamidronate
Parvo B19
IF- alpha
Primary FSGS mx
75%
Steroids 1mg/kg/day
End of 4 months resistance
Total 6-8 months
Resistant people-cyclosporin
Or tacrolimus
25%
Asymptomatic
ACE inhibitors and ARB
Salt restricted diet
Drugs tried in patients with FSGS with questionable benefits
MMF
Cyclophosphamide
Galactose
HIVAN is called
HIV associated nephropathy
Increased viral loads
Absolute indication to start on HART
apo L1 polymorphism
Characters of collapsing FSGS
collapse of glomeruli + hypertrophy
Pseudocresent–podocytes containing protein resprbtion droplets
Dilated tubules + microcyst
EM– tubulo reticular inclusion bodies
IF Footprints
