Robbins Ch. 20 - The Kidney I Flashcards
CVA location
T12-L1
-location of renal colic
tubules and interstitium
toxic/infection
glomeruli
immunologic
acute kidney injury
most damage - proximal tubules
rapid decline in GFR**
reversible
chronic kidney disease
GFR decreased to <60 for at least 3 months
OR persistant albuminuria
irreversible
nephrocalcinosis
calcification of the renal parenchyma
ESRD
GFR < 5% normal
end stage
podocyte
in lamina rara externa of BM
subendothelial
cations - cross BM
subepithelial
anions - cannot cross BM
GFR reduce to 30-50% of normal
slow progression to ESRD
cycle of FSGS
pocodyte loss > increased proteins in mesangium > proliferation of mesangium > ECM accumulation > segmental sclerosis > global sclerosis
TGF-beta
mediator of sclerosis
better correlate with kidney fxn
tubulointerstitial damage
subendothelial deposits?
lupus nephritis
MPGN
epimembranous deposits?
membranous nephropathy
subepithelial deposits?
acute GN
mesangial deposits?
IgA nephropathy
group A beta hemolytic strep
post-strep GN
SpeB
post-strep GN antigen
granular subepithelial humps, IgG/C3, hypocomplementemia
post-strep GN
post-strep GN treatment?
95% children recover with salt/water balance
non-streptococcal GN
Hep B/C, malaria, staph
staph ?
IgA deposits
untreated RPGN
death within weeks to months
crescent formation
RPGN
-proliferation of parietal and visceral epithelium
prognosis of RPGN
with steroids - many still need dialysis
alpha4 of collagen IV
goodpastures
-cross react with alveolar tissue
HLA-DRB1
associated with goodpasture
Tx of goodpasture
plasmapharesis
IgG/C3 linear deposits
anti-GBM antibody mediated disease
- goodpastures
- type of RPGN
immune complex deposition RPGN
postinfectious GN, lupus nephritis, IgA nephropathy, henocy schonlein
granular deposit
Tx - underlying disease
ANCAs
pauci immune
-type of RPGN
50% of RPGN
have type 3 - pauci immune
oval fat bodies
in urine - nephrotic syndrome
majority of nephrotic in children
caused by primary disease (95%)
majority of nephrotic in adults
caused by secondary disease (systemic) - DM, SLE, amyloidosis
nephrotic syndromes?
membranous glomerulopathy
minimal change disease
FSGS
PLA2R
membranous glomerulopathy
diffuse thickening of glomerular cap wall
membranous glomerulopathy
subepithelial, granular, IgG/C3, spike appearnace
membranous glomerulopathy
non-selective proteinuria
membranous glomerulopathyF
FSGS
selective proteinuria
minimal change disease
IgG4
membranous glomerulopathy
HLA-DQ1
membranous glomerulopathy association
thyroiditis
membranous glomerulopathy
prognosis of membranous glomerulopathy
40% transplant recur
40% to ESRD
women, low proteinuria - best prognosis
hodgkins lymphoma
minimal changes disease
most common cause of nephrotic in children
minimal change disease
-no deposits - only effacement of foot processes
minimal change disease Tx?
reversible with corticosteroid therapy
most common cause nephrotic in adults?
FSGS, primary
secondary FSGS
HIV, heroin, sickle cell, obesity, renal abloation
FSGS prognosis
bad - 50% ESRD within 10 years
25-50% transplants recur
mutations in slit diaphragm?
podocin
nephrin
alpha-actinin 4
TRPC6
IgM/C3, non-selective proteinuria
FSGS
HIV associated nephropathy
FSGS collapsing variant
- bad prognosis
- fical cystic tubule dilation - full of proteinacious material
nephritic syndromes?
acute proliferative GN (post-strep, post-infectious)
RPGN