Glomerulonephritis and nephritic syndrome Flashcards
what do we see in GN and nephritic syndrome and what do they mean?
- hematuria- blood in urine
- oliguria- reduced GFR
- azotemia- elevated BUN/creatinine
- HTN
Glomerular hematuria looks like
muddy brown blood- “coca-cola”
urine analysis in GN can look like either _____ and ________
WBC/cellular casts and RBC casts/dysmorphic RBC
pathogenesis of glomerulonephritis
- glomerular injury
- influx of inflammatory cells
- glomerular inflammation
immune mediated glomerular injury steps
- immune complex deposition, ab, and activated neutrophils - with/without complement activation
- influx of inflammatory cells and remodeling GBM
- Glomerular injury/symptoms
Glomerulonephritis can be caused by (5)
- acute post-streptococcal/postinfectious
- Membranoproliferative
- Crescentic
- IgA nephropathy/ Henoch-Schonlein purpura
- SLE
acute post-streptococcal/postinfectious
- caused by
- most commonly after
- pathogenesis
- Gn presents
- caused by deposition of immune complexes
- most common after- strptococcal pharyngitis (group A beta-hemolytic Strep)
- pathogenesis: - subendothelial antigen (ag) depostion during infection anad antibody (ab) delivery during immune phase - subendothelial deposition of circulating Ag-Ab complexes
- GN presents 1-3 weeks after infection
acute post-streptococcal GN is a prototype for acute post-infectious GN:
- other infections include
- most frequent in
- treatment?
- recovery?
- impetigo - endocarditis - abscess -osteomyelitis
- most frequent in children
- no specific treatment
- most children recover without complications within 3 months
Membranoproliferative GN:
- _____ glomerular inflammation
- caused by
- pt. presents with
- results in
- most cases are secondary to
- Type I/ primary MPGN is
- presents in ______ with a nephritic presentation with _____ complement
- chronic glomerular inflammation
- caused by deposition of immune complexes in subendothelium and in the GBM
- pt. presents with chronic inflammatory or autoimmune disorders
- results in GBM abnormalities and inflammatory changes
- most cases are secondary to hepatitis
- Type I/ primary MPGN is idiopathic
- presents in young adults with a nephritic presentation with low complement
Cresentic Gn:
- what is the crescent signify
- indicates
- patient presents with
- it is a finding not a diagnosis
- indicate severe glomerular inflammation with destruction of glomerular capillary wall
- clinically the patient presents with rapid loss of kidney function- RPGN
Anti-GBM disease:
- autoimmune disorder with
- etiology
- trigger
- if ab against GBM cross reacts with alveolar GM in the lung it is
- autoimmune disorder with circulating anti-GBM ab
- etiology is ?
- trigger viruses/toxins in susceptible individual
- if ab against GBM cross reacts with alveolar GM in the lung it is goodpasture syndrome (pt. will present with hemoptysis)
if negative pauci-immune
granulomatosis with polyangitis- Wegner’s
Pauci-immune GN:
- most common cause of
- Ab to
- ANCA activates _______ in the capillaries causing endothelial injury and vasculitis (inflammation of the blood vessel)
- most common cause of crescentic GN
- Ab to neutrophils cytoplasmic antigens (ANCA)
- ANCA activates neutrophils in the capillaries causing endothelial injury and vasculitis (inflammation of the blood vessel)
IgA Nephropathy and Henoch-Schonlein Purpura (HSP)
- ____ deposition disease; when it is in the systemic capillaries and vessels it is ____ and when it is in the glomeruli only it is ________
- most common
- age
- recurrent
- IgA deposition disease; when it is in the systemic capillaries and vessels it is HSP and when it is in the glomeruli only it is IgA nephropathy- Berger disease
- most common primary GN in the world: 10% in the USA and 40% in Asia
- age: early childhood and adolescence
- recurrent microscopic or gross hematuria
Lupus Nephritis:
- what is wrong
- which organ is involved 50%
- true or false: morphologic and clinical presentation is variable
- immune complex deposition in glomeruli/vessels
- Kidney is involved 50%
- True
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pt with acute post-streptococcal-postinfectious GN notice the cellular glomerulous
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pt with acute post-streptococcal-postinfectious GN notice the inflamed glomerulous
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pt with acute post-streptococcal-postinfectious GN- IF shows granular deposits of IgG and complement C
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pt with acute post-streptococcal-postinfectious GN- EM notice that the subepithelial deposits are under the podocytes
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pathogenesis of acute post-streptococcal-postinfectious, MPGN and immune complex deposition related GN
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biopsy of a pt with membranoproliferative GN
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pt with membranoproliferative GN notice the thick wall of the capillary and the inflammatory cells
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pt with membranoproliferative GN notice the thick and double contours of rhe GBM
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pt with membranoproliferative GN- chronic depositions of IgG and complement C3
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pt with membranoproliferative GN notice the subendothelial electron dense deposits
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Crescentic GN
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Ig linear-smoky or vapor like- seend in Anti- GBM disease or goodpasture syndrome
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IgG granular seen in immune complex deposition
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ANCA positive vasculitis- no immunoglobin
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against collagen iv causing inflammatory cells to enter
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immune complex deposition related Gn EM and also seen in Lupus Nephritis
pathogenesis of pauciimmune GN notice the neutrophils that are granular and bilobar- granules cntain peroxidase and proteinases which when Ab attack activates them which causes destruction of capillaries and endothelium leading to injury
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HPS
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IgA nephropathy notice the increased mesengial matrix in response to the IgA deposition
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IgA nephropathy
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IgA nephropathy notice the electron dense deosits corresponding to IgA depositions
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Lupus nephritis
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