Fibrine et fibrinoïde dans les glomérulopathies. Etude comparée en pathologie expérimentale et spontanée

Abstract

The presence of fibrinoid substance in the capillary loops following glomerular lesions of diverse etiologies has given rise to the hypothesis of an identical pathogenesis. An electron microscope study was made of the mode of formation of the fibrinoid substance and of its role in the development of chronic lesions. Macromolecules, like liquoid (Roche) and antibody-antigen complexes with thrombocytes initiate the formation of intra-capillary fibrin in parenchymatous tissues, particularly in the kidney, in the absence of previous lesions of the endothelium. This fibrin degrades and takes on a granular aspect typical of that of fibrinoid sub-stance. The endothelium and the intercapillary cells react to this deposit of fibrin by tumefaction followed by proliferation. If these lesions are allowed to evolve, their electron micrographs present images of sub-acute and chronic nephritis. Numerous counterproofs point to fibrin and fibrinoid as the agents responsible for the lesions and their subsequent development. Electron micrographs of biopsy material from 3 patients suffering from glomerular nephropathies of different etiologies are absolutely the same as those of the experimental lesions. In all cases undergraded fibrin and fibrinoid substances were demonstrated. Thus in both spontaneous and experimental pathologies the formation of fibrin, which implies a process of intravascular coagulation, is an indispensable step in the genesis of numerous glomerulopathies.