Path - Kidney Flashcards
Acute/Diffuse Proliferative GN, Post-Strep/Infectious GN
Clinical Finding = Pathogenesis = LM = EM = IF =
Acute/Diffuse Proliferative GN, Post-Strep/Infectious GN
Clinical Finding = Nephritic Syndrome
Pathogenesis = Immune Complexes, Circulating or Planted Ag’s
LM = Enlarged and Hypercellular Glomeruli, Diffuse Proliferation, Leukocyte Infiltration, Crescents if severe
EM = Subepithelial, Electron Dense Deposits or “Humps”
IF = Focal, Granular IgG and C3 in GBM and mesangium (IgA if Staph aureus)
What clinical presentation would you expect to see in a Patient with Acute/Diffuse Proliferative GN; Post-Strep/Infectious GN?
Most Commonly 6-10yo Child w/ sudden onset malaise, fever nausea, periorbital edema, mild to moderate HTN, Oliguria, Subnephrotic Proteinuria, Dysmorphic RBC’s/Casts, and Hematuria 1-2 weeks following Group A Beta Hemolytic Strep Pharyngitis
Worse prognosis in Adults, likely to happen suddenly without infection. Only 60% will recover quickly, rest will progress to Chronic GN or RPGN
Goodpasture Syndrome
Clinical Finding = Pathogenesis = LM = EM = IF =
Goodpasture Syndrome
Clinical Finding = Nephritic Syndrome; Type I RPGN/Crescentic GN/Exudative GN/Extra-Capillary GN
Pathogenesis = Anti-COL4-A3 (a3 chain of Type IV Collagen)
LM = Extracapillary proliferation with crescents, Necrosis
EM = GBM disruption, Fibrin, no deposits
IF = Linear IgG and C3, Fibrin in crescents
What clinical presentation would you expect to see in a Patient wil Goodpasture Syndrome?
Young Male, HLA-DRB1, RPGN,
Wegener’s Granulomatosis (Granulomatosis w/ Polyangiitis) and/or Microscopic Polyangiitis (Leukocytoclastic/HSN Vasculitis)
Clinical Finding = Pathogenesis = LM = EM = IF =
Wegener’s Granulomatosis (Granulomatosis w/ Polyangiitis) and/or Microscopic Polyangiitis (Leukocytoclastic/HSN Vasculitis)
Clinical Finding = Type III RPGN/Crescentic GN/Exudative GN/Extra-Capillary GN
Pathogenesis =
LM = Extra-capillary proliferation with crescents, necrosis
EM = GBM Disruption, Fibrin, no deposits
IF = None
What clinical presentation, outcome, etc. might you expect from a patient with RPGN?
Severe Oliguria
Severe Glomerular Injury
Death in Weeks to months if untreated
If they survive acute episode, more than 90% will progress to Chronic GN
Prognosis is poor
Type I may be treated with Plasmaphoresis
What type of things can cause Type II RPGN?
What will be their staining on IF?
Post-Infectious GN, SLE, IgA Nephropathy, or HPS can lead to Type II RPGN
They will show Granular IF Deposition of Immune Complexes
Minimal Change Disease (MCD)
Clinical Findings = Pathogenesis = LM = EM = IF =
Minimal Change Disease (MCD)
Clinical Findings = Nephrotic Syndrome Pathogenesis = Unknown LM = Normal EM = Effacement of Podocyte Foot Processes IF = None
What are some of the Characteristic Clinical features of Minimal Change Disease?
- Most Common Cause of Nephrotic Syndrome In Children
- Excellent Response to Steroids
- There is some sort of association with Respiratory Infection, Immunizations, and Hodgkins Lymphoma
- Preserved Renal Function without Hematuria, HTN, or Decreased GFR despite Massive Proteinuria
- Selective Proteinuria
- Good Prognosis
FSGS
Clinical Findings = Pathogenesis = LM = EM = IF =
FSGS
Clinical Findings = Nephrotic Syndrome
Pathogenesis = Unkown; Ablation Nephropathy
LM = Focal, Segmental Sclerosis and Hyalinosis
EM = Effacement of Podocyte Foot Processes; Sclerosis
IF = Focal; IgM and C3
What are some of the characteristic Clinical features of FSGS?
- Most Common cause of Nephrotic Syndrome in Adults IN THE US, especially in blacks and Hispanics
- Associated with HIV, Heroin Addiction, Sickle Cell Disease
- Differs from MCD: increased Hematuria and HTN, decreased GFR, Non-Selective Proteinuria, Poor Response to Steroids
- 50% will progress to ESRD, Poor Prognosis, Renal Transplant or Dialysis is inevitable
