Renal Path 10/28 (lots of Glomerular Nephritis) Flashcards
Autosomal dominant PCKD?
Adult
Berry aneurysms
Adult PCKD
Mitral valve prolapse
Adult PCKD
Autosomal recessive PCKD?
Enlarged, smooth kidneys
Childhood
7% of dialysis patients with acquired cystic develop?
renal cell carcinoma
The BIG feature of glomerulonephritis?
IMMUNE MEDIATED
complement C5a molecule does what?
chemotactic for neutrophils
“Diffuse” GN means:
all glomeruli involved
“focal” GN means:
a portion of glomeruli involved
“Global” GN means:
entire single glomerulus involved
“Segmental” GN means:
part of single glomerulus involved
some component of the kidney is the antigen?
in situ immune complex deposition
antigens and antibodies form complex before deposit in kidney:
circulating immune complex deposition
LINEAR, homogenous, diffuse pattern on IF:
Anti-GBM GN
Pulmonary alveoli involvement GN
Goodpastures
NC1 domain of alpha 3 chain of type IV collagen is antigen
Anti-GBM GN
Granular, interrupted pattern on IF
M-type Phospholipase A2 antigen
Membranous GN
Heymann
Inflammatory and Proliferative GN
Nephr-I-tic syndrome
Proteinuria > 3.5 g/24 hrs
Nephr-O-tic syndrome
Low serum C3
Large hypercellular glomeruli
subEPIthelial “Camel Humps” on EM
Acute Poststreptococcal GN
“smoky” urine
periorbital edema
children
Acute poststreptococcal GN
Crescents (fibrinous proliferations) of parietal epithelial cells of Bowman’s capsule mixed with inflammatory cells
Rapidly Progressive GN
RPGN
LINEAR deposits in IF
Type I
anti-GBM
RPGN
“lumpy-bumpy” granular pattern on IF
Type II
Immune complex mediated
RPGN
lack of IF staining
pANCA or cANCA
Type III
Pauci-immune
Time frame for RPGN
Weeks
Complement mediated damage to GBM
“SPIKES” on silver stain
Membranous GN
Most common cause of nephrotic syndrome in children
Minimal Change Disease
Atopy (prone to allergic rxn)
Hodgkin Lymphoma
Minimal Change Disease
Tx for minimal change disease?
corticosteroids
**responds well!!!
Diffuse Effacement of Foot Processes and no deposits on EM
no IF staining
normal glomeruli
Minimal Change Disease
Main lab finding in MCD?
MASSIVE proteinuria
sclerosis of SOME (not all) gloms
HIV
HEROIN
Sickle cell
Morbid Obesity
Focal Segmental Glomerulosclerosis
FSGS
Pathogenesis of FSGS:
damage to visceral epithelial cells
On light microscopy:
Collapsed GBM
increased mesangial matrix
hyalinization
+/- foam cells
FSGS
proteinaceous material and inflammation
tubuloreticular inclusions in endothelial cells
HIV nephropathy
leukocyte infiltration
mixed nephrotic/nephritic
Membranoproliferative Glomerulonephritis
SLE
Hep B/C
Endocarditis
Infx vetriculoarterial shunts
Hematologic malignancy
Membranoproliferative Glomerulonephritis
“tram track” on silver stain
MPGN
SUBENDOTHELIAL deposits on EM
Alternative complement pathway
Type I MPGN
“Dense deposit disease”
-lamina densa of GBM is “RIBBON LIKE”
Type II MPGN
Most common glomerulonephritis worldwide
IgA Nephropathy
recurrent hematuria
maybe gluten enteropathy or liver disease related
IgA Nephropathy
Site of IgA deposition in IgA Nephropathy?
mesangium
MESANGIAL DEPOSITS OF IGA ON I.F.
IgA nephropathy
Hematuria following respiratory, GI, or urinary tract infx:
IgA nephropathy
Nephritis
nerve deafness
eye disorders
Alport Syndrome
Irregular “thick and thin” GBM
splitting of lamina densa
Alport Syndrome
COL4A5
defective GBM synthesis
Alport Syndrome
Diffuse thinning of GBM
Thin Membrane Disease
Small, diffusely granular kidneys
Globally hyalinized glomeruli
Chronic GN
Disease most likely to progress to Chronic GN?
RPGN (crescentic)
“Full house” – IF stains with everything
“Wire loop” lesions
Lupus Nephritis
IgA in mesangium
Purpuritic skin lesions
HSP