Ultrastructure of transplant glomerulopathy.
Thirty-one specimens of tissue were obtained from 15 renal allografts 3-96 months after transplantation and studied by light, electron and in some cases also by immunofluorescence microscopy. All patients had a degree of renal insufficiency and almost all had proteinuria and moderate  hypertension; nephrotic syndrome was present in one and hematuria in two. On histological examination one patient showed cellular proliferation suggestive of glomerulonephritis (recurrent or de novo) and another patient had numerous crescents. The most frequent glomerular lesion was widening of the lamina rara interna with subendothelial accumulation of finely granular material, formation of new subendothelial basement membrane and deposition of microfibrils and fine filaments. The mesangial changes were mainly those of mesangiolysis and mesangial sclerosis with deposition of mesangial matrix and microfibrils, but little cellular proliferation. Fragmented red blood cells were seen in nearly half of the patients. In another seven patients the lesion resembled focal segmental glomerulosclerosis. This combination of changes termed transplant glomerulopathy leads to diffuse glomerular sclerosis. Arterial intimal thickening and occasionally also thrombosis produced ischaemic changes in the kidney and in the glomeruli and contributed significantly to the process of transplant rejection.
D001158:Arteries / Q000473:pathology; D003599:Cytoskeleton / Q000473:pathology; D005260:Female; D006801:Humans; D007674:Kidney Diseases / Q000209:etiology / Q000473:pathology*; D007678:Kidney Glomerulus / Q000648:ultrastructure*; D016030:Kidney Transplantation; D008297:Male; D008854:Microscopy, Electron; D008856:Microscopy, Fluorescence; D011183:Postoperative Complications; D014184:Transplantation, Homologous; D014652:Vascular Diseases / Q000473:pathology