GN Flashcards
glomerular disease is diagnosed by?
biopsy! (pathological, not clinical dx)
three types of microscopy used to examine renal biopsies
light + staining, immunofluorescence, electron
three types of cells in the glomerulus
podocyte (epithelial), endothelial cell, mesangial cell (at the neck)
fenestrated endothelial cell is separated from the podocyte by?
glomerular basement membrane
primary sx of nephrotic syndrome
edema, proteinuria, hypoproteinemia, hyperlipidemia, lipiduria (with oval fat bodies in urine)
primary sx of nephritic syndrome
hematuria, azotemia, HTN, RBC casts
major causes of nephrotic syndrome
minimal change GN, FSGS, membranous glomerulopathy, diabetic nephropathy, amyloidosis, (membranoprolif, lupus)
major causes of nephritic syndrome
IgA nephropathy, lupus GN, IgA vasculitis, cryoglobulinemic vasculitis, anti-GBM GN, ANCA GN (membranoprolif)
what does minimal change glom look like on microscopy?
normal by LM, normal by IM, foot process effacement on EM
who gets minimal change glom?
children
tx of minimal change glom
corticosteroids (empiric in a kid, don’t need biopsy first)
what does membranous glom look like on microscopy?
thick capillary walls on LM, granular capillary wall staining on IM, dense subepithelial deposits on EM (these are immune complexes)
primary membranous glom is caused by?
anti-phospholipase A2 receptor auto-antibodies (antigen comes from podocyte)
secondary causes of membranous glom
SLE, infections (hep B, syph), metal drugs, malignancy
what does FSGS look like on microscopy?
parts of some glomeruli have consolidation of glomerular tufts
primary FSGS is _____; secondary causes include?
idiopathic; HIV, mutation in podocyte genes, drug toxicity (heroin, pamidronate, interferon-alpha), adaptive structural response (obesity, sickle cell, congenital heart disease)
what does membranoproliferative glom look like on microscopy?
thick capillary walls AND hypercellularity (from leukocyte infiltration), variable IM based on immune complex vs. dense deposit dz
causes of immune complex MPGN
chronic bacterial infection (osteomyelitis, endocarditis), hep C (cryoglob), malignancy
causes of dense deposit MPGN
abnormalities in alternative complement pathway activation (antibodies or mutations)
most common cause of ESRD in US
diabetic glomerulopathy
signs of diabetic nephropathy
proteinuria, progressive decline in GFR, HTN
what does DN look like on microscopy?
progressive thickening of GBM, increase in mesangial matrix, KW nodules
which types of amyloid cause nephrotic syndrome?
AL amyloid, AA amyloid
by EM, amyloid looks like?
randomly arranged fibrils
name three types of glomerulonephritis that cause nephritic syndrome
immune complex (granular), anti-GBM (linear), ANCA (no IF)
name the major patterns of glomerular injury
mesangioprolif, prolif (inside lumen), crescent (extracapillary), sclerosing (order of severity)
order glomerulonephritis in order of severity
acute postinfectious, IgA < lupus (huge range) < ANCA, anti-GBM
acute postinfectious GN most often presents with what pathological features
diffuse proliferative GN with PMNs inside the lumen, subepithelial humps, and granular staining on IF
the primary reason for a renal biopsy of a patient with SLE is to?
assess disease severity and direct management
class V lupus shows what histologic manifestations?
membranous GN, thick BM
IgA nephropathy has IgA dominant ____ immune deposits
mesangial (so mesangioprolif GN is common presentation)
when IgA vasculitis is systemic, it is called?
Henoch-Schonlein purpura
systemic vasculitis from Hep C is called?
cryoglobulinemic vasculitis
ANCA GN and vasculitis is due to antibodies against?
myeloperoxidase or proteinase 3 (proteins in cytoplasm of PMNs and monocytes)
pathology of ANCA GN
capillary necrosis and rupture, leading to crescent GN
ANCA associated pulm lesions
hemorrhagic (hemoptysis), granulomatous, or eosinophilic inflammation
when ANCA strictly affects the kidneys only, it is called?
Pauci-Immune Crescentic GN
why doesn’t ANCA-GN show up on IF
ANCA directly attacks cells rather than the membrane
in anti-GBM disease, patients have antibodies against?
type IV collagen in the GBM (leads to linear IF staining)
ANCA GN presents in a (younger/older) population
older
measurement of proteinuria
24-hour urine collection, spot urine-creatinine ratio (should be less than 0.2)
transient proteinuria can occur in the present of ?
fever
proteinuria must be ____ in order to suspect glomerular disease
fixed
complications of nephrotic syndrome
thrombosis! (due to loss of anticoag factors) – can be DVT or renal vein thrombosis; infection (due to loss of Ig); accelerated atherosclerosis
clues that hematuria is glomerular
brown color, proteinuria, dysmorphic RBCs (acanthocytes especially), RBC casts, rash
GN associated with low C3 (alternative pathway)
postinfectious, endocarditis, membranoprolif.
GN associated with low C3 and C4 (classic pathway)
lupus, cryoglobulinemic
GN associated with normal complement levels
ANCA, IgA nephritis, Henoch-Schonlein purpura, Goodpasture’s
signs of necrotizing vasculitis
systemic, skin, respiratory, and ENT symptoms
