Non-inflammatory and Inflammatory Glomerular diseases Flashcards
Nephritic Syndrome
Clinical presentation of inflammatory glomerulonephritis
- Microscopic hematuria
- Proteinuria
- Hypertension
- Edema
Nephrotic syndrome
Clinical presentation of non-inflammatory glomerulopathy
- Proteinuria (>3.5g/d)
- Hyperlipidemia
- Edema
- Hypoproteinemia
- Urinalysis is key to diagnosis
Complications of nephrotic syndrome
- Hypercoag
- Edema
- infection
- Accelerated atherogenesis
Histopath of minimal change disease
Everything is normal (light, silver stain, immunofl) except electron microscopy which shows podocyte effacement
Etiology of minimal change disease
Unknown but can be secondary to NSAIDs or neoplasms
Treatment of minimal change disease
Steroids, podocytes look normal
Light micro: FSGS
- Focal, segmental sclerosis
- Segmental collapse with adhesions to bowman’s cap
- Podocyte injury loss
Immunofl: FSGS
-IGM and C3 in collapsed mesangium
EM: FSGS
-Podocyte effacement, hyalin accumulation in cap loops–>collapse
Causes of FSGS
Podocyte injury leadin got proteinuria and glomerulosclerosis
What is the point of no return?
When about 40% of podocytes are lost, get global sclerosis
What attenuates podocyte loss and scarring?
RAAS inhibition
Why is podocyte injury so bad?
Don’t regenerate, leads to scarring and decreased GFR
Membranous glomerulopathy histology: PAS/silver stain
Sclerosis with basement membrane spikes
Membranous glomerulopathy histology: Trichrome
Sub epithelial proteinaceous deposits
Membranous glomerulopathy histology: Immunofl
IgG and C3 in the granular capillary loop
Membranous glomerulopathy histology: EM
- Podocyte effacement
- Subepi electron dense deposits
- New BM surrounding immune complex deposits
Most common antibody found in membranous glomerulopathy?
M-type PLA2R
Secondary etiology of Membranous glomerulopathy
- Infectious: Hep B, C, malaria etc
- Neoplasms
- Meds (gold salts, penicillamine)
- Lupus
What is glomerular inflammation a response to?
Final common response to capillary injury–>scar
Steps of programmed response to capillary injury
- Holes/cap wall injury
- Proliferation (WBCs enter tufts)
- Acellular crescent formation (ECM fills bowman’s)
- Cellular crescent formation (cells in matrix produce scar)
- Glomerular and interstitial scarring
Mechanisms that result in capillary injury?
- Antibody mediated
- Immune complex deposits
- Mechanism X (vasculitis)
Good pastures disesase
antibody mediated pulmonary-renal synrome with hemoptysis and RPGN
Differential diagnosis for pulmonary-renal syndrome?
Good pastures, lupus, ANCA small v vasculitis
Good pastures in light micro
- Hypercellular glomerulus
- Firbin
- Crescents in bowman’s space
Good pastures in immunofl
- Linear GBM stain
- Stringy fibrin in bowman’s
Good pastures in EM
- Compressed glomerular tuft
- Fibrin in bowman’s
- No complexes
Treatment of Good pastures
- Plasma exchange
- Immunosupp
- Rituximab
Post-strept GN
Immune complex mediated disease around 21 days post-strept with RPGN
Post-strept GN light micro
- Diffuse, proliferative exudative GN
- Increased PNMs/glomerular cells
- Occasional subepi deposits
- Accentuated lobular structure
Post-strept GN immunofl
Granular IgG, C3
Post-strept GN EM:
- large subepi deposits
- no sclerotic rxn
- subepi and mesangial deposits
Lupus nephritis
Immune complex with RPGN, can also present with nephrotic syndrome
Lupus nephritis Immunofl
“Full house pattern” stains for all
-granular cap and mesangial loop
Lupus nephritis LM
- Prolif in mesangium or lots of prolif everywhere
- WIRE LOOPs=thick cap loops
- Subendo deposits or epith
Lupus nephritis EM
- Mesangial, subepi and sub endo deposits
- Effaced podocytes
IgA nephropathy
Immune complex disease that is slowly progressive with edema and gross hematuria (usually non-systemic)
systemic version of IgA nephropathy
Henoch Schoenlein purpura (HSP)
- Systemic vasculitis in childhood
- RPGN, rash, colitis, arthritis
IgA nephropathy light M
- Hypercellularity in mesangium
- Focal crescents
IgA nephropathy immunofl
Granular in mesang, igA and C3
IgA nephropathy EM
Mesangial electron dense deposits
ANCA-Associated SV Vasc
Pauci-immune GN (mech X) that mimics common diseases
ANCA-Associated SV Vasc light M
Vasculitis with fibrinoid necrosis
necrotizing focal GN with crescents
ANCA-Associated SV Vasc siver stain
focal crescents, segmental necrosis (loss of BM)
ANCA-Associated SV Vasc Fl and EM?
None
