nephritis path
anti-GBM
pathogenesis
histology
immunofluorescence
immune complex glomerulonephritis
post-streptococcal glomerulonephritis
lupus nephritis
IgA nephropathy
ANCA-associated vasculitis
nephrotic path
minimal change disease
focal segmental glomerulosclerosis
primary
genetic
secondary
HIV-associated nephropathy ("collapsing FSGS")
membranous nephropathy (aka membranous glomerulopathy, membranous GN)
subendothelial (cause of hypercellularity and inflammation) and subepithelial deposits (podocyte dysfunction, not a nephritic picture)
histologic findings
subepithelial/intramembranous deposits (against the podocyte), causes GBM changes.
silver stain only marks collagen IV of GBM, so there are spaces between spikes. These are not actual spaces, but deposits that are visualized on trichrome staining.
etiologies
clinical findings
lupus
malignancies
infections
hep B
hep C
drugs
histologic findings
hypercellularity
dsDNA very specific for lupus nephritis, ANA positive is less specific