Renal - Immune Mediated Diseases Of Kidney

Front 1

Nephrotic syndrome:
Most common causes?(3)

5 major symptoms?

Why does the glom get affected by inflammation?

Back 1

Acute post-strep GN
Anti-GBM nephritis
Lupus nephritis, vasculitis

hematuria, proteinuria, edema, oliguria, reduced renal fxn

capillary network, enormous blood volume, high pressure, directs MHC I, II molecules

Front 2

Most common form of primary GN worldwide:

defined by presence of _____ and to a lesser extent ____ in the glom.

main cause of _______ in pts who require renal replacement.

Glom deposits are what subtype of IGA?

Back 2

IGA nephropathy

presence of IGA, lesser extent C3

ESRD

IGA1

Front 3

Some IGA nephropathy pts have elevated serum levels of IGA in complex with _________.

________ is seen in over 35% of transplant recipients.

IGA nephropathy: decreased clearance of IGA1 by _________.

IGA-mediated vasculitis, purpuric rash on legs/butt, abd pain, renal lesions:

Back 3

fibronectin

RES

Henoch-Schonlein purpura

Front 4

Anti-GBM GN:
strong association with _______.

Anti-GBM Ag's (type ____) are directed to _______ collagen.

Anti-GBM + pulmonary hemorrhage:

Back 4

HLA-DR2

IGG - Type IV

Goodpasture's

Front 5

What cells are routinely found in the tissue infiltrates of Anti-GBM?

Blood levels of ______, a marker for T-cell activation, are increased.

what alters permeability at the GBM, causing proteinuria, secreted by the T-cells?

Back 5

Activated T-cells (Th1-CD4+)

sIL2-R (CD25)

lymphokines

Front 6

Pro-inflammatory cytokines made produced by macrophages:

How do macrophages link innate and specific immunity?

Back 6

TNF-a, IL-1, IL-6, IL-12

act as APC's for B-cells, T-cells

Front 7

When does a post-infectious GN usually appear?

What gets deposited in tissues? Hypersensitivity type?

What forms in situ? Hypersensitivity type?

Post-infectious GN - activates what pathway?

Back 7

7-10 days post infection

circulating Ag-Ab complexes - Type III

in situ - immune complexes with bacterial ag's - Type II

alternative complement

Front 8

Post-infectious GN:
renal biopsies show deposits of ____, ____, sometimes ____.

What are two "candidate" nephritogenic antigens?

What do you use to treat?

Back 8

renal biopsies - C3, IGG, sometimes IGM

endostreptosin, strep exotoxin B

PCN, erythromycin

Front 9

Lupus nephritis:
What type of hypersensitivity?

Intense local complement activation --> ___ C3,4 in circulation.

Tx for lupus nephritis?

Back 9

Mixed Type II,III

low C3,C4

prednisolone

Front 10

non-immune mediated GN, causes bystander damage to glom endothelial cells:

Biopsies from Wegener's show _____ immune deposits.

What causes Wegener's?

C-ANCA characterized by staining cytoplasm for __________.

Back 10

Wegener's granulomatosis

little to no immune deposits

presence of C-ANCA (anti-neutrophil cytoplasmis auto-Ab's_

proteinase 3

Front 11

P-ANCA characterized by staining cytoplasm for _______.

ANCA-neutrophil interaction close to capillary triggers _________.

T/F: ANCA titers correlate with disease activity.

Back 11

myeloperoxidase

endothelial damage

True

Front 12

Cryoglobulinemia:
essential cryoglobulinemia characterized by large ____________ on the vessel walls.

Causes? (4)

What Ab is predominantly present?

Back 12

deposits of Ag-Ab complexes

viral/bacterial infections
Non-Hodgkin's lymphoma
SLE
Hep C

IGG

Front 13

Any GN characterized by crescents in Bowman's capsule:

presence of crescents in gloms is a marker for ________.

Types:
Anti-GBM?
Immune complex mediated?
Non-immune mediated?

Back 13

RPGN

severe injury

Anti-GBM - Goodpasture's
Immune complex - IGA, post-strep, SLE
Non-immune - Wegener's