Pathology Of Rejection Part I (Mostly Humoral)

Front 1

Injury in Rejection can be direct immune mediated resulting in injury to

Back 1

Tubules and interstitium, Blood vessels (vasculitis), Glomeruli (glomerulitis)*

Front 2

Injury in Rejection can be indirect immune mediated resulting in

Back 2

Vascular injury resulting in ischemia

Front 3

what are the mechanisms of antibody mediated rejection?

Back 3

Antibodies ‐ either those pre
existing or subsequently
produced bind to alloantigens
on vascular endothelial
cells. This recruits inflammatory cells to the site of binding

Front 4

Describe how the anitbodies can cause acute rejection

Back 4

In acute rejection, mediators
of acute inflammation are
recruited and the vascular
wall can be damaged quickly
with resulting thrombosis.

Front 5

What is the direct pathway of cellular rejection?

Back 5

Direct pathway:
Initially, donor-derived
antigen presenting cells
(dendritic cells, DC)
present antigen and result
in an immune response.

Front 6

This is what:
Initially, donor-derived
antigen presenting cells
(dendritic cells, DC)
present antigen and result
in an immune response.

Back 6

Direct pathway of cell mediated rejection

Front 7

what is the indirect pathway of cell mediated rejection?

Back 7

Indirect pathway:
Later, host-derived
antigen presenting
cells participate in
generating the immune
response.

Front 8

The mononuclear cells
injuring blood vessels
and tubules can be
identified in biopsies of what?

Back 8

Acute rejection via cell mediated processes

Front 9

now understood to have both cellular and humoral components

Back 9

chronic rejection

Front 10

immediate ‐minutes (even seconds) to hours rejection is called

Back 10

Hyperacute

Front 11

Longer than “hyperacute” but more quickly than acute rejection is referred to as

Back 11

Accelerated acute

Front 12

abrupt decline in function after weeks to months describes what

Back 12

Acute rejection

Front 13

Gradual decline in fxn after months to years describes

Back 13

chronic rejection

Front 14

Antibody‐mediated rejection can manifest as what two types of rejection

Back 14

acute humoral rejection and Hyperacute rejection

Front 15

In antibody mediated rejection describe the appearance of the tubbules interstitium and blood vessels

Back 15

In the tubules there is ischemic injury and necrosis but tubulitis is not common, in the interstitium one sees edema and hemorrhage but there is a lack of mononuclear infiltrate, and in the vessels on see a sever vasculitis manifesting as fibrinoid necrosis.

Front 16

The morphologic features seen
in “hyperacute” and accelerated acute” rejection are usually dramatic and are highly suggestive of

Back 16

AQntibody mediated rejection

Front 17

What does the kidney look like grossly in the antibody mediated rejection of hyperacute and accelerated

Back 17

the kidney is enlarged buldging, and has discolored areas that represent infarction

Front 18

Severe acute humoral
rejection is characterized by

Back 18

ischemic necrosis consequence of vascular
thrombosis

Front 19

consequence of vascular
thrombosis seen in severe acute humoral rejection

Back 19

ischemic necrosis

Front 20

When less dramatic, humoral rejection cannot be

Back 20

diagnosed on the basis of morphology alone.
• Problem: Antibodies cannot be directly visualized!

Front 21

this is a marker for the prescence of antibody mediated rejection

Back 21

The demonstration of C4d (an inactive product of the breakdown of C4) in peritubular capillaries

Front 22

The demonstration of C4d (an inactive product of the breakdown of C4) in peritubular capillaries

Back 22

this is a marker for the prescence of antibody mediated rejection

Front 23

closely associated with the presence of donor
specific antibodies

Back 23

C4d

Front 24

acute rejection is currently
the best “direct” evidence in
biopsy specimens of
Antibody-mediated
rejection.

Back 24

The presence of C4d in
acute rejection is currently
the best “direct” evidence in
biopsy specimens of
Antibody-mediated
rejection