Kidney Transplantation

Arteritis, Intimal (synonymous with endothelialitis)
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
Arteritis, Transmural
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
Borderline Changes
Changes which might be considered suggestive of rejection but which are nondiagnostic (such as a moderate interstitial mononuclear cell infiltrate with very mild tubulitis)
De novo Glomerulonephritis
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
Hyperacute Rejection
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
Ischemic Glomerulopathy
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
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
Persistence of lesions which were present in the transplanted kidney before transplantation, such as, glomerulonepheritis. This should not be mistaken for recurrence
Transplant Glomerulopathy
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
Infiltration of tubular epithelium by leukocytes, usually lymphocytes
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.

Please mail comments, corrections or suggestions to the TPIS administration at the UPMC.