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histopathology of the kidney (intro to histo of kidney (glomerulus ( image…
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glomerular diseases
inflammatory
nephritic syndrome
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RBC pathology
RBC casts
dysmorphic RBCs
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anti-GBM disease
histology
LM: extracapillary proliferation (crescents), fibrinoid necrosis
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EM: compressed glomerular tuft, no electron dense deposits
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Pauci-immune GN
pathogenesis: pathogenic Ab produced, binds to intracellular antigens in neutrophils --> PMNs degranulate in small vessels
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non-inflammatory
nephrotic syndrome
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minimal change disease
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EM: podocytes demonstrate extensive foot process effacement. No capillary loop electron dense protein (immune) deposits. Normal GBM. Mesangium has normal cellularity, matrix and no electron dense deposits.
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etiologies
primary
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? circulating factor, B or T cell mediated
secondary
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tx: stop offending agent, treat underlying condition, consider steroids
membranous nephropathy
anti-PLA2R + MN
phospholipase A2 receptor is present in normal podocytes and in immune deposites in patients with idiopathic MN. PLA2R and IgG4 co-localize on biopsy specimen from pts with idiopathic MN in a typical granular pattern
histology findings
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IF
granular staining for IgG, C3, kappa and lambda (can also stain for PLA2R in kidney biopsy)
EM
subepithelial electron dense deposits and podocyte foot process effacement
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tx: ACEI or ARB, immunosuppression (cyclophosphamide, calcineurin inhibitors, rituximab)