Renal Flashcards
What are the 4 comparetments of renal disease?
glomeruli
tubules
interstitial
blood vessels
chronic renal disease eventually gets all 4
what is azotemia?
elevation of BUN and creatinine due to decreased GFR
what is prerenal azotemia?
azotemia due to hypoperfusion , CHF, volume depletion, shock
what is postrenal azotemia?
azotemia due to outflow obstruction
what is uremia?
the symptoms of azotemia
what is nephritic syndrome?
hematuria and some proteinuria and hypertension due to glomerular injury
what is nephrotic syndrome?
> 3.5 g/day proteinuria, hypoalbuminemia, edema, hyperlipidemia due to glomerular injury
what is rapidly progressive glomerulonephritis?
nephritic with rapid decline in GFR
what if hematuria or proteinuria is asymptomatic?
mild glomerular injury
what is acute tubular injury?
rapid decline in GFR resulting in azotemia, injury to any compartment
what is CKD?
chronic kidney disease significant GFR reduction lasting >3 months
this is the end stage
what is ESRD?
end stage renal disease
<5% GFR
what are renal tubular defects?
tubule disorders that show up as polyuria and electrolyte abnormalities
what is the difference between primary and secondary glomerulonephritis?
primary-glomeruli are the guy
secondary-other systemic disease
what are the pathologic responses to glomerulus injury?
hypercellularity
basement membrane thickening
hyalinosis and sclerosis
diffuse/focal/global lesions
why does glom injury have hypercellularity?
proliferation of mesangials/endothelials
infiltration of leukocytes
glomerular epithelial prolif
why does glom injury have BM thickening?
depositiion of immune complexes, fibirin, amyloid, etc
why does glom injury have hylainosis and sclerosis?
hyalinosis-endothelial inury –> plasma proteins come in
sclerosis –> damage –> deposition of collagen
what causes most glomerulonephritis?
immune compexes, Ig deposition
what is the antigen in renal epithelium that causes lots of GN? what happens when antibodies bind?
M-type phospholipase A2 (PLA2r)
immune complexes cause basement thickeing and a granular pattern (heymann nephritis)
what occurs in antibodies against planted antigens?
basically antigens from other stuff get stuck in kidney then antibodies come and do damage
discrete granular pattern
what is antibody induced GN?
autoimmune disease, antibodies directed against normal components of the GBM
example: goodpasture syndrome
what is goodpasture syndrome? staining pattern?
auto abs bind to a3 chain of type IV collagen in glomerular basement membrane–> linear staining pattern –> leads to nephritic syndrome, azotemia, oliguria, HTN
how does gGN result from deposition of immune complexes? stain?
complexes get trapped –> Fc receptors activate complement –> damage to subendothelial, subeithelial, mesangial
granular pattern
where do immune complexes normally deposit and what determines that?
determined by size/charge
cationic –> crosses GBM and forms sub-epithelial complexes
-non inflammatory
anionic –> trapped in sub-endothelium
-inflammatory
neutral –> mesangium
large –> get eaten by macros before they can do damge
sm
how does cell mediated GN work?
T cells do stuff
how does complement do damage?
C3 directed GN
what are the mediators of glomerular injury?
cells -neutros, monos, -macros -plateletes -resident glomerular cells (mesangial) soluble mediators -complement 5b-9 MAC -eicosanoids, NO, AT, endothelin -cytokines, IL1, TNF -chemokines-PDGF and TGFb -coag proteins-fibirin
what cell type is injured in glomerular disease that cant regenerate?
podocytes –> causes them to detach from BM
neprin and podocin mutations can also do this w/o inflammation
what occurs in focal segmental glomerulosclerosis? (also in FA)
usually via systemic HTN –> increase GBF/filtration/pressure –> endothelial injury –> protein accumulation –> macros come –> increase matrix synthesis
rest of good glomeruli compensate by hypertrophying to make up for the ones that suck –> then they eventually undergo same fate
