Glomerular changes in renal allografts.
The renal allograft is host to a number of injuries and all its structural components are prone to damage. The glomeruli respond to these varied stimuli in many ways. The fibrinoid necrosis, thrombosis, and polymorphonuclear cell exudation that accompany hyperacute or accelerated rejection are well-recognized. The transplant may also be afflicted by forms of de novo or recurrent glomerulonephritis. Apart from these, there are other patterns of reaction. The mesangium is often the site of a rapidly reversible change; it expands readily. Arterial changes initiate ischemia and collapse of glomerular capillary spaces. Glomerulitis accompanies cases of acute rejection, but when seen as a predominant feature, usually antedates chronic rejection. Heavy proteinuria may be associated with profound alterations in the peripheral capillary basal lamina including irregular thickening, interposition of mesangial cell cytoplasm, and lamellation. Allografts with these glomerular changes eventually fail.
D001485:Basement Membrane / Q000473:pathology; D001706:Biopsy; D005920:Glomerular Mesangium / Q000473:pathology; D006084:Graft Rejection; D006801:Humans; D007678:Kidney Glomerulus / Q000473:pathology*; D016030:Kidney Transplantation; D008854:Microscopy, Electron; D014184:Transplantation, Homologous