Glomerular Filtration Barrier (GFB) IMMUNE COMPLEX DEPOSITION

- Blocks passage of RBCs, WBCs, and proteins

POST-STREPTOCOCCAL GLOMERULONEPHRITIS

Nephritic Syndrome  1-2 wk/s status post-strep infection

- GBM damage  leakage of RBCs, WBCs, proteins
Nephrotic syndrome
- Damage in the podocytes  proteinuria (>3.5
g/day)
 Anti-ASO / Anti-DNAse B antibodies  subepithelial
deposition (b/w podocytes and GBM)  activates
complement system (C3-6)  GBM damage 
inflammation
 C3 consumption
 Leads to renal failure
SSSSSSS
 Causes rapidly progressive glomerulonephritis
(RPGN)

NEPHRITIC SYNDROME
IgA Vasculitis
1. Hematuria
- RBC casts  Most common nephritic syndrome
o RBCs take on the shape of the kidney  1-2 days status post URTI or GIT infection
tubules  IgA deposit in mesangium  GBM damage 
- Acanthocytes leakage of RBC, WBC, and protein into urine 
2. Proteinuria (<3.5 g/day – subnephrotic range) inflammation
3. WBCs in urine (Sterile pyuria) o No complement activation
 Skin complication: SSSSSSS
o Purpura on butt
CAUSES OF NEPHRITIC SYNDROME  GIT complication:
o Abdominal pain
1. Anti-GBM Disease (Good pasture syndrome)
 Joint:
- Hemoptysis + Hematuria
o Arthralgia
- Anti-GBM antibody damages GBM
- Leakage of RBC, WBC, protein  Causes rapidly progressive glomerulonephritis
(RPGN)

Lupus Nephritis

 Have history of lupus

 Malar or discoidal rash, anemia
 Cells damaged  release antigens  bind to
antibodies (anti-nuclear antibodies, anti-double
stranded DNA antibodies)  sub-endothelial and
sub-epithelial immune complex deposition  C3
complement activation  C3 consumption  GBM
damage
 Nephrotic range proteinuria
 Causes rapidly progressive glomerulonephritis
(RPGN)

Membrano-proliferative Glomerulonephritis

 Does not cause rapidly progressive

glomerulonephritis (RPGN)
 Primary is idiopathic
 Secondary is caused by Hepa B, C viruses and
cryoglobulinemia
 Subendothelial deposition