Glomerulopathies in human renal allografts.
The present study discusses the light, electron and immunofluorescence microscopy as well as some clinicopathologic correlations of rejection change in human renal allograft glomeruli. It is based on examination of 126 tissue specimens from 54 grafts obtained from 50 patients (1966-1973). The most frequent and characteristic lesion was membranous transplant glomerulopathy (MG) with irregular fibrillar thickening of capillary walls but without conspicuous hypercellularity. This thickening was caused by subendothelial depositsdifferent from classical fibrinoid lesions. During further progression, widening and peripheral extension of mesangium with degenerative changes became apparent. Advanced MG was encountered most frequently in the 2nd year after transplantation (TPL) at moderate to medium proteinuria and hypertension. It was accompanied by endarteristic rejection changes, and renal insufficiency set on usually in the course of the 3rd year. Nevertheless, the course, symptoms, and graft survival exhibited considerable variations. - The morphology and manifestations of destructive segmental transplant glomerulopathy  (SG) depended on the time of its development. In the early stage (within about 3 months after TPL), the lesion was characterized by areas of fibrinoid insudation and necro(bio)sis associated with severe vascular changes, most frequently obliterative arterio(lo)pathy (OA). The ultrastructure was characterized by endothelial defects with host's polynuclear reaction and focal intravascular coagulation. The grafts thus affected failed soon, their function usually subsiding within the first trimester  at a moderate, but gradually increasing proteinuria and severe persistent hypertension. The late from of destructive SG presenting as fibrohyaline obliteration of the loops with foam cells always accompanied advanced MG with severe arterial lesions. - Fluorescence microscopy revealed both linear and focal fixation of antisera, which, however had no apparent correlation with the microscopical and clinical presentations.
D001485:Basement Membrane / Q000473:pathology; D002196:Capillaries / Q000473:pathology; D004727:Endothelium; D005455:Fluorescent Antibody Technique; D006084:Graft Rejection; D006801:Humans; D006977:Hypertension, Renal / Q000209:etiology; D007136:Immunoglobulins / Q000032:analysis; D007678:Kidney Glomerulus / Q000276:immunology / Q000473:pathology* / Q000648:ultrastructure; D016030:Kidney Transplantation; D011507:Proteinuria / Q000209:etiology; D013997:Time Factors; D014184:Transplantation, Homologous / Q000009:adverse effects
D007136:Immunoglobulins