102914 glomerular disease Flashcards
mechanisms of glomerular disease
immunocomplex deposition-ciruculate then deposit in glomerulus(like lupus). activates complement resulting in neutrophil chemotaxis
antibodies against GBM or glomerular antigens
cytokine production by inflam cells
glomerular disease that is diffuse is
affecting all glomeruli
focal
affects a few glomeruli
global
affects the entire glomerulus
segmental
affects a portion of the glomerulus
how does glomerular disease present?
loss of GFR
hematuria
proteinuria
nephrotic syndrome
proteinuria greater than 3.5 g/day
hypoalbuminemia
edema
hyperlipidemia
lipiduria
hypercoagulability
nephritis
mild proteinuria
HEMATURIA (RBCs, RBC casts, dysmoprhic RBCs)
HTN
edema
nephrotic glomerular diseases
minimal change disease
focal segmental glomerulosclerosis
membranous nephropathy
IgA neprhopathy
nephritic glomerular diseases
membranoproliferative GN
acute post infec GN
crescentic (ANCA) GN
IgA nephropathy
acute glomerulonephritis causes
IgA nephropathy post infec GN anti GBM disease/Goodpasture's small vessel vasculitis lupus nephritis membranoproliferative GN
what is the most common GN?
IgA nephropathy
in what disease does hematuria frequently occur with an URI? (synpharyngitic hematuria)
IgA nephropathy
what is a histologic feature of IgA nephropathy?
IF: mesangial IgA deposition
HSP
systemic disorder with IgA deposition in multiple organs (skin, joints, GI, kidney)
oliguria
low urine output
histology findings for post Strep GN
EM: mesangial and large subepithelial hump-like deposits of immune complexes
rapidly progressive GN
nephritic syndrome with rapid progression (in days to weeks) to renal failure
causes of rapidly progressive GN
anti-GBM/Goodpasture’s
immune complex GN
ANCA associated GN (pauci immune)
how do you diagnose anti GBM/Goodpasture’s?
anti GBM Ig in blood
LINEAR IgG and C3 on kidney biopsy IF
pauci immune GN
crescenteric GN with little deposition of immune reactants (as opposed to anti-GBM disease, IgA nephropathy, lupus nephritis)
idiopathic or associated with ANCA vasculitis
what do RPGNs look like under light microscopy?
crescenteric GN
IF microscopy of immune complex mediated RPGN?
variable deposition of immune complex and complement
IF microscopy of pauci immune RPGN?
negative
nephrotic syndrome from primary renal disease ex
membranous nephropathy
focal segmental glomerulosclerosis
minimal change disease
in children, 80% have minimal change disease
secondary causes of nephrotic syndrome include
systemic diseases-diabetes mellitus, SLE, amyloidosis
infections
drugs-NSAIDs
what is the most common cause of nephrotic syndrome in children
minimal change disease
minimal change disease in adults can be caused by
idiopathic or
drugs-NSAIDs
neoplasms-Hodgkin’s lymphoma
infections
minimal change disease histology
LM: glomeruli, interstitium and tubules look NORMAL
EM: podocyte foot process effacement (fusion)
membranous nephropathy-what secondary causes are responsible for it?
infections-HBV
connecive tissue diseases-SLE
neoplasms-carcinoma of lung, colon, stomach, breast. Non-Hodgkin’s lymphoma
drugs
membranous nephropathy histology
LM: diffuse thickening of GBM. GBM spikes on silver stain
membranous nephropathy
immune deposits form on subepithelial aspect of glomerular basement membrane
forms of focal segmental glomerulosclerosis
primary (acute onset nephrotic syndrome)
secondary
hereditary
causes of secondary FSGS
drugs-NSAIDs
infections-HIV
etc
FSGS histology
LM: focal and segmental glomerular sclerosis with capillary collapse
in terms of glomerular diseases, SLE can cause
a number of different ones
