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Definitions
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Arteritis, Intimal (synonymous with endothelialitis) |
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Intimal thickening with inflammation of arterial subendothelial space
ranging from rare intimal inflammatory cells to necrosis of endothelium
with deposition of fibrin, platelets and inflammatory cells. The
cellular infiltrate is composed of lymphocytes and monocytes. Severity
is determined by the number of vessels affected as well as by intensity
of individual lesions. Mild degrees of initmal arteritis can be
extremely focal
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Arteritis, Transmural |
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Injury and inflammation of the whole arterial wall including the media,
necrosis of medial smooth muscle cells, fibrin insudation and cellular
infiltration with mononuclear as well as polymorphonuclear leukocytes
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Borderline Changes |
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Changes which might be considered suggestive of rejection but which
are nondiagnostic (such as a moderate interstitial mononuclear cell
infiltrate with very mild tubulitis)
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De novo Glomerulonephritis |
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Glomerulonephritis in the allograft morphologically dissimilar to the
original disease and distinct from transplant glomerulopathy or transplant
glomerulitis. Presumed to be due to etiologies similar to those
responsible for native kidney glomerulonephritis
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Hyperacute Rejection |
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Rejection presumed to be due to preformed antibody, usually characterized
by polymorph accumulation in glomerular and peritubular capillaries at one
hour post-transplant with subsequent endothelial damage and capillary
thrombosis
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Ischemic Glomerulopathy |
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A. Acute: glomerular capillary engorgement and glomerular necrosis.
May occur in hyperacute and in severe acute rejection. B. Late:
thickening, wrinkling and collapse of glomerular capillary walls associated
with extracapillary fibrotic material. May be a sequel to diffuse arterial
occlusion in chronic vascular rejection
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Recurrence |
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Lesions in the graft morphologically similar to the original disease,
and presumed to be due to persistence of pathogenetic mechanism leading
to end stage disease in the native kidney, such as, diabetic
glomerulopathy, recurrent glomerulonephritis, and amyloidosis
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Transmission |
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Persistence of lesions which were present in the transplanted kidney
before transplantation, such as, glomerulonepheritis. This should not be
mistaken for recurrence
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Transplant Glomerulopathy |
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Immunologic glomerular damage due to transplant antigens.
A. Early form (glomerulitis): Endocapillary accumulation of lymphocytes
and monocytes with endothelial cell swelling.
B. Late form (syn. chronic transplant glomerulopathy): Mesangial cell
proliferation, peripheral mesangial interposition and sometimes cellular
cresents. The late form is usually associated with marked proteinuria, often
in the nephrotic range. Should be distinguished from ischemic glomerular
change, recurrent glomerulonephritis and transmitted glomerulonephritis
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Tubulitis |
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Infiltration of tubular epithelium by leukocytes, usually lymphocytes
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Reference
Solez, K, et al. International standardization of criteria
for the histologic diagnosis of renal allograft rejection: The Banff
working classification of kidney transplant pathology.
Kidney Int 1993;44(2):411-22.
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