Serum and Urinary Fibrin/Fibrinogen Degradation Products in Glomerulonephritis

Origin of Urinary Fibrin-Fibrinogen Degradation Products in Renal Glomerular Disease

“…As has been found in previous studies, serum FDP levels were within normal limits [Clarkson et a!., 1971;Ekert et al, 1972], indicating that the major part of the urinary FDP is not derived by the direct filtration of FDP circulating in the plasma. Thus in patients with renal glomerular damage causing heavy non-selective proteinuria, most of the urinary FDP arise by the direct filtration of plasma fibrinogen through a damaged and abnormally permeable GBM.…”

“…1975. Renal diseases that do not cause marked proteinuria are seldom associated with a marked increase in urinary FDP excretion [McNicol et al, 1971;Hall, 1975], However, controversy persists as to whether urinary FDP arise by the lysis of intraglomerular fibrin deposits [Clarkson et al, 1971: Heelner et al, 1974: Ekberg and Pandoffi, 1975 or by the filtration of fibrinogen (and FDP) through a damaged and abnormally permeable GBM [Ekert et al. 1972;Cortes et ai, 1973 or whether both mechanisms may operate concur rently in some conditions.…”

“…It is widely held that urinary FDP arise from the lysis of intraglomerular fibrin deposits [Clarkson et al, 1971;Hedner et al, 1974: Ekberg andPandolfi, 1975;Hedner, 1975]. However, other groups [Ekert et al, 1972;Cortes et al, 1973;Hall et al, 1975] have produced evidence that urinary FDP arise by the differential filtration of plasma fibrinogen and FDP through a damaged and abnormally permeable glomerular basement membrane (GBM).…”

What Is the Evidence for Activated Coagulation in Glomerulonephritis ?

“…The demonstration of FDP in urine of patients with GN commanded great interest since FDP are known to promote inflammation [9]. Furthermore, an important role of fibrin and FDP has been suggested in the genesis of proliferative GN and particularly crescent formation [10].…”

Role of Plasminogen Activator Inhibitor on Nephrotoxic Nephritis and Its Modulation by Tumor Necrosis Factor

“…An imbalance between coagulation and fibrinolysis in the development of glomerulonephritis is suggested by the deposition of fibrin in the glomerular capillaries [1,2] and by the finding of fibrin degradation products in the urine and serum [3]. The effects of intraglomerular coagulation in the induction of glomerulonephritis may be to reduce glomeru lar function [1,4], promote leukocyte chemotaxis [5] and pathophysiologic conditions may be responsible for the thrombogenesis of endothelial cells in vitro [11] and for recurrent venous thrombosis in vivo [12].…”