The pathogenetic role of the coagulation process in glomerular diseases of immunologic origin.
The experimental and clinical observations analyzed in this review suggest that the deposition of fibrin within glomeruli is an important pathogenic mechanism in the series of events leading to progressive destruction of glomerular capillaries. Neither the causal factors nor the consequences of this type of reaction are peculiar to the glomerulus. Fibrin deposits can occur in any injured blood vessel and, if not rapidly dealt with by fibrinolysis, will lead to endothelial changes and the development of organizing thrombi. It seems that glomerular capillaries are especially vulnerable; there are several reasons for this. First, some immunologic reactions are triggered within the glomeruli and thus produce a local inflammatory response, leading to fibrin deposition. Secondly, the glomerular filtration function allows a progressive local accumulation of potentially damaging particles, such as circulating fibrinogen derivatives (formed during generalized intravascular clotting), or phlogistic immune complexes (as a result of systemic antigen-antibody interaction); these too cause local injury and fibrin deposition. Finally, the glomerular obliteration resulting from the organization of such fibrin deposits leads to irreversible damage and so has more serious implications for the patient than if the lesions occurred elsewhere, where the formation of functionally useful new capillaries is often possible. It seems reasonable to propose, therefore, that the use of anticoagulant may be natural therapy in cases with the risk of rapid, massive, and continuous fibrin accumulation in glomeruli, where glomerular sclerosis and irreversible renal failure are likely.
D000925:Anticoagulants / Q000494:pharmacology; D000936:Antigen-Antibody Complex; D000937:Antigen-Antibody Reactions; D001485:Basement Membrane / Q000276:immunology / Q000473:pathology; D001777:Blood Coagulation; D001778:Blood Coagulation Disorders / Q000209:etiology; D004211:Disseminated Intravascular Coagulation / Q000473:pathology; D004697:Endocarditis, Bacterial / Q000150:complications; D005337:Fibrin / Q000378:metabolism; D005921:Glomerulonephritis / Q000209:etiology / Q000276:immunology; D006801:Humans; D006818:Hyalin / Q000378:metabolism; D007674:Kidney Diseases / Q000473:pathology / Q000503:physiopathology*; D007678:Kidney Glomerulus / Q000187:drug effects / Q000276:immunology / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D008180:Lupus Erythematosus, Systemic / Q000150:complications; D010587:Phagocytosis; D011693:Purpura / Q000150:complications
D000925:Anticoagulants; D000936:Antigen-Antibody Complex; D005337:Fibrin