Jan9 M3-Introduction to Renal Pathology Flashcards
4 main compartments of the kidney
glomeruli, tubules, interstitium, vasculature
arterial-venous system in the kidney
arteries: renal, interlobar, arcuate, lobular, afferent, efferent
capillaries: network under capsule + peritub drain in stellate veins. vasa recta drain in arcuate vein
veins: stellate veins-lobular veins-arcuate veins-interlobar-renal
normal podocytes on EM
can distinguish individual podocytes and see the space between them
2 types of glomerular barriers to proteins
size-selective (large proteins and blood)
charge-selective (albumin): BM is negatively charged
selective vs non selective proteinuria + indicates what + particular thing in non-selective
- selective = albumin only = alteration of negative charge
- non selective = not albumin only = anomaly to endoth or GBM or podocytes. can see hematuria
pathological consequence of the glomerulus being part of our (micro)vasculature
anything that injures small blood vessels affects it (diabetes, htn, vasculitis, thrombosis)
glomerulus is a site of predilection for the deposition of ________ and this is the major form of ________
immune complexes. major form of GN
problem in GN nomenclature
many types of glomerular diseases have no inflammatory cells
immune vs non immune glomerular injury
immune: often bx, antibody mediated, in situ complex formation or deposition of preformed complexes
non-immune: nephron loss, injury to podocytes, no bx
give 2 immune mediated GNs
anti GBM disease
membranous nephropathy
anti GBM disease pathophgy
CIRCULATING antibodies attack type IV collagen in GBM: leads to inflam rx
membranous nephropathy pathophgy
de novo antibodies attack structures near the podocytes
2 types of diseases where deposition of preformed circulating immune complexes exists + where they deposit
-endocarditis and post infection rheumatic
-lupus (SLE)
Deposit on glomerulus
what determines the location where preformed circulating immune complexes deposit (2) + where do they deposit
- their size and their charge
- the balance of Ag to Ab
Deposit on the glomerulus
type of non immune mechanism of glomerular disease
hyperfiltration injury
hyperfiltration injury: 2 main reasons it happens
adaptive changes in glomeruli (hypertrophy + GC htn) and systemic htn
pathophgy of hyperfiltration injury and how disease detected
GC htn, G hypertrophy and systemic htn lead to epithelial and endo injury and proteinuria
what is the glomerulus’ reponse in hyperfiltration injury and what is typically seen
glomerulosclerosis (mesengial cells prolif, ECM prod, intraglom coagulation, vessels obliterated, tubules and interstitium disappear and become fibrotic)
what happens to tubules and interstitium in hyperfiltration injury
they disappear and become fibrotic
why is there a vicious circle in hyperfiltration injury
glomeruli that aren’t injured try to compensate so they become hypertrophic and hyperfiltrate so buildup of GC pressure
to what extent is hyperfiltration injury reversible
to some extent until too much fibrosis
causes of hyperfiltration injury
htn, diabetes, GN, cystic kidney disease
9 major renal syndromes
- asymptomatic proteinuria
- nephrotic syndrome
- asymptomatic hematuria
- nephritic syndrome
- rapidly progressive GN
- AKI
- CKD
- UTI
- nephrolithiasis (stones)
first test performed on nephro patient and when to check urine sediment
dipstick. when dipstick positive for anything
dipstick checks what
blood hemolyzed, non-hemolyzed, protein, glucose, pH, WBCs, ketones, etc.
urine sediment checks for what (4)
cells, casts, crystals, organisms
nephritic syndrome main features
hematuria, RBC casts, MILD-MODERATE proteinuria, htn
RBC casts: how they’re formed and sign of what
RBCs pass glomerulus and compact in the tubules.
cast = sign of glomerular injury
nephrotic syndrome lab features (5 classical)
HEAVY proteinuria (>3g) Hypoalbuminemia Hyperlipidemia Lipiduria Severe edema
PURE nephrotic syndrome on bx
no cellular proliferation, inflammation, necrosis or crescent formation
does finding RBCs in the urine = glomerular problem?
no. casts yes. but blood can come from anywhere in urinary tract until urethra
nephrotic syndrome urinary sediment features
fatty and hyaline casts, lipids, oval fat bodies (shedded tubular cells filled with lipids)
3 modalities used on renal bx
LM, immunofluorescence(IF), EM
what is done in renal bx LM other than usual H&E (2)
other stains to outline GBM and mesengium (silver, PAS, trichrome, ..)
3 things that immunofluorescence on renal bx gives us
- negative or positive for immune complex and Ig presence
- location (mesengium, capillary wall)
- patterns: (linear vs granular)
3 main things EM tells us on renal bx
- location and appearance of deposits
- appearance and thickness of GBM
- evaluation of podocytes
4 ways a glomerulus can react in GN
- hypercellularity and proliferation of mesengial, epith, inflam cells
- necrosis
- GBM thickening
- sclerosis (scarring)
what hypercellularity and proliferation rx of glomerulus shows
there is an inflammatory cell component
what’s a crescent
proliferation of parietal epithelial cells of Bowman’s capsule often associated with glomerular necrosis
what crescents show
severe glomerular injury, necrosis, GBM destroyed
acute vs chronic crescents
acute: cellular crescent
chronic: fibrous crescent
4 words in glomerular lesion nomenclature and def
focal: some glomeruli
diffuse: most glomeruli
segmental: part of glomeruli
global: entire glomerulus
segmental vs gobal sclerosis or hypercel or wtv: definition
segmental: <50% of glomerular tuft (of the glomerulus)
global: >50%
exudative injury to the glomeruli meaning
hypercellularity + too many neutrophils
