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