Late failure or human renal transplants. An analysis of transplant disease and graft failure among 125 recipients surviving for one to eight years.
The purpose of the present paper was to study clinical, morphological and immunological aspects of late rejection of renal allotransplants. We have, therefore, analyzed the occurrence and nature of renal transplant disease and graft failure among 125 recipients surviving for 1 to more than 8 years after transplantation. In this population transplant disease as defined by the appearance of heavy proteinuria and/or steadily declining graft function occurred in 22 patients. At the closure date of the study on December 31, 1972 complete graft failure had occurred in 12 of these 22 patients and 4 of these have died. In addition two patients died in the presence of normal graft function, due to chronic hepatitis and metastatic cancer respectively. As based on clinical findings, pathophysiological features and renal lesions the patients with late transplant disease were classified into two groups and described accordingly. Group A, termed glomerular transplant disease, included a majority of 16 patients, constituting a rather homogenous idsease entity in relation to course of disease, clinical findings and renal lesions as studied by light-, immunofluorescence- and electron microscopy. All these patients presented with heavy proteinuria, which was non-selective in all but two, resulting eventually in complete loss of graft function in eight cases. All these patients developed hypoalbuminemia and hypercholesterolemia, and one half manifested a classical nephrotic syndrome. Arterial hypertension occurred in all patients except two. Glomerular structure as studied by light microscopy revealed a number of lesions of a rather polymorphous pattern in all patients in group A. Endomesangial proliferation, hyperplasia and segmental proliferation of epithelial cells and thickening of capillary walls were prominent features, although the degree of severity, extension and type of lesion occurred in such varying proportions that classification into any well characterized category of glomerulonephritis was not possible. All cases in group A revealed immune deposits, most frequently containing IgG, IgM, complement and fibrinogen. IgA, IgD and IgE were also demonstrated in a lesser proportion of cases in this group. The immunofluorescent pattern was a mixed granular and linear, and in no case strictly linear or granular alone. The ultrastructural investigation contains a detailed analysis of the
D000328:Adult; D000743:Anemia, Hemolytic / Q000150:complications; D001707:Biopsy, Needle; D003718:Denmark; D005260:Female; D005500:Follow-Up Studies; D005921:Glomerulonephritis / Q000503:physiopathology; D006084:Graft Rejection / Q000150:complications*; D006087:Graft vs Host Reaction; D006650:Histocompatibility Testing; D006801:Humans; D007676:Kidney Failure, Chronic / Q000601:surgery; D007678:Kidney Glomerulus / Q000473:pathology; D016030:Kidney Transplantation; D008297:Male; D008856:Microscopy, Fluorescence; D008875:Middle Aged; D009395:Nephritis, Interstitial / Q000150:complications; D009400:Nephrosclerosis / Q000150:complications; D011507:Proteinuria / Q000209:etiology; D012709:Serum Albumin; D014184:Transplantation, Homologous
D012709:Serum Albumin