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
pt with acute post-streptococcal-postinfectious GN notice the cellular glomerulous
pt with acute post-streptococcal-postinfectious GN notice the inflamed glomerulous
pt with acute post-streptococcal-postinfectious GN- IF shows granular deposits of IgG and complement C
pt with acute post-streptococcal-postinfectious GN- EM notice that the subepithelial deposits are under the podocytes
pathogenesis of acute post-streptococcal-postinfectious, MPGN and immune complex deposition related GN
biopsy of a pt with membranoproliferative GN
pt with membranoproliferative GN notice the thick wall of the capillary and the inflammatory cells
pt with membranoproliferative GN notice the thick and double contours of rhe GBM
pt with membranoproliferative GN- chronic depositions of IgG and complement C3
pt with membranoproliferative GN notice the subendothelial electron dense deposits
Crescentic GN
Ig linear-smoky or vapor like- seend in Anti- GBM disease or goodpasture syndrome
IgG granular seen in immune complex deposition
ANCA positive vasculitis- no immunoglobin
against collagen iv causing inflammatory cells to enter
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
HPS
IgA nephropathy notice the increased mesengial matrix in response to the IgA deposition
IgA nephropathy
IgA nephropathy notice the electron dense deosits corresponding to IgA depositions
Lupus nephritis
