Microangiopathic Haemolytic Anaemia and Scleroderma
Renal damage may result from glomerular fibrin deposition. This occurs in some forms of glomerulo-nephritis and can cause, for example, capsular crescent formation (Figures 13.1 and 13.2) and local scarring in some segmental proliferative lesions. Deposition of fibrin may be precipitated by antigen- antibody complexes whichare capable of releasing thrombogenic substances from platelets, and this probably explains its association with immunologically-mediated diseases such as glomerulonephritis. However, intravascular coagulation induced by other non-immunological mechanisms may also result in glomerular fibrin deposition. The associated changes in the glomeruli have been elegantly demonstrated in rabbits by Vassalli et al.1 and include endocapillary cell proliferation, capsular crescent formation, leukocyte infiltration, deposition of fibrin and its derivatives (seen ultrastructurally as deposits of varying electron density) in the mesangium and the widened sub-endothelial space, and swelling of endothelial cells.
KeywordsHaemolytic Uraemic Syndrome Afferent Arteriole Progressive Systemic Sclerosis Microangiopathic Haemolytic Anaemia Glomerular Tuft
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- 1.Vassaili, P., Simon, G. and Rouiller, C. (1963). Electron microscopic study of glomerular lesions resulting from intravascular fibrin formation. Am. J. Pathol., 43, 578–617.Google Scholar
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