Glomerulonephritis Flashcards
Nepritic syndromes characteristics/signs
- classic presentation of pts w/glomerulonephritis
- reduction of GFR ==> elevated serum creatinine
- hematuria + dysmorphic RBCs and/or RBC casts + proteinuria
- WBCs also possible
- hypertension + edema
Typical renal-limited diseases associated w/glomerulonephritis
- IgA nephropathy
- Anti-GBM disease
- Membranoproliferative glomerulonephritis (MPGN)
- Renal limited vasculitis (ANCA associated)
- Hemolytic-uremic syndrome
- C3 glomerulopathy/Dense deposit disease
Typical systemic diseases associated w/glomerulonephritis
- Henoch-Schönlein Purpura
- Goodpasture’s syndrome
- Lupus nephritis
- ANCA associated vasculitis
- Infection associated
- Post-infectious
- Endocarditis/shunt nephritis
- Cryoglobulinemia
- Immunoglobulin deposition diseases
Common labs/serology evaluation in glomerulonephritis
- lab: CBC, electrolyte, 24-hour urine, liver fxn tests
- serology:
- C3 (complement) levels
- antistreptolysin (ASO) titer
- ANA, ANCA, cryoglobulins, anti-GBM
Pulmonary-renal syndrome definition
- patients presenting w/glomerulonephritis + pulmonary hemorrhage
- e.g. in Goodpasture’s or ANCA-associated vasculitis
Blood tests + disease associations in glomerulonephritis
ANA, Anti-DS DNA
Lupus
C3, C4
See table
Blood cultures
Bacterial endocarditis
ASO
Post-infectious
Hepatitis C
Cryoglobulinemia
Hepatitis B
Membranoproliferative glomerulonephritis
Anti-neutrophil cytoplasmic antibodies (ANCA)
Pauci-immune vasculitis
Anti-GBM antibodies
Anti-GBM disease, Goodpasture’s syndrome
Pathophysiology of proteinuria in glomerulonephritis
- direct damage to glomerular capillary wall via immunologic mechanisms ==> increased protein filtration
Pathophysiology of reduction of GFR in glomerulonephritis
- reduced GFR <== acute, inflammatory process w/in glomerulus
- ==> glomerular vasocontsriction/occlusion or thrombosis ==> decreased filtration surface area
Pathophysiology of active urine sediment in glomerulonephritis
- excretion of RBCs, WBCs, or casts <== glomerular inflammation + disruption of GBM
Pathophysiology of edema/hypertension in glomerulonephritis
- edema <== increase in tubular reabsorption of salt + water <== reduced glomerular perfusion w/normal tubular fxn ==> expansion of ECF volume
- HTN <== salt + water retention
Epidemiology/etiology: Post-infectious glomerulonephritis
- occurs 2-3 wks after Group A strep infection
- most common in children
- may occur w/acute or subacute active infections
- mediated by Ab response to strep ==> immune complex deposition + activation of complent @ glomeruli
Pathology/Clinical Presentation: Post-infectious glomerulonephritis
- light microscope: proliferative + exudative w/inflitration of PMNs and monocytes
- Immunofluorescence: IgG + C3 deposits @ subendothelial, mesangial, subepithelial
- clinical present:
- edema + sudden weight gain + HTN
- hematuria + proteinuria
- decreased GFR
- Positive ASO titer
- decreased C3 w/normal C4
Diagnosis/Tx: Post-infectious glomerulonephritis
- Dx: nephritic syndrome + positive streptozyme + low C3
- Tx: supportive
Epidemiology/etiology: IgA Nephropathy
- most common; usually males 15-35
- mediated by deposition of IgA complexes @ mesangium ==> activation of mesangial cells ==> cell proliferation
Pathology/Clinical: IgA Nephropathy
- light: increase in mesangial cell number/matrix
- IF: IgA, IgG, C3 @ mesangium
- Clinical:
- usually asymptomatic
- often increased hematuria w/onset of viral illness
- systemic sx possible
- skin w/IgA deposits = Henoch-Schonlein purpura