Immunofluorescent Localization of Antihemophilic Factor Antigen and Fibrinogen in Human Renal Diseases

Macrophage-induced glomerular fibrin deposition in experimental glomerulonephritis in the rabbit.

“…Thus glomerular PCA appears to activate the extrinsic coagulation pathway, as does macrophage PCA. Macrophage-induced GFD via PCA would thus explain the observations of Hoyer et al (42).…”

“…Studies by Hoyer et al (42) assessing renal tissue from patients with GN and prominent fibrin deposition failed to demonstrate the presence of Factor VIII. This finding suggested that the intrinsic coagulation pathway was not involved in fibrin deposition in human GN.…”

Idiopathic Rapidly Progressive Glomerulonephritis

“…Fibrinogen and fibrin polymers are present be tween the cells of crescents and in Bowman's space in all cases ( fig. 1) [32], but factor VIII is absent suggesting a thrombin-independent mechanism for fibrin deposition [47], Linear deposits of IgG, accompanied in about 50% of cases by C3, suggest anti-GBM disease which can usually be confirmed by serum studies (see below) [38]. Occasion ally, IF findings may be helpful in identifying crescentic glomerulonephritis due to another less severe primary renal disease such as IgG-IgA nephropathy [32, 42,45,46] or anti-GBM disease complicating membranous nephrop athy [3,[48][49][50], In occasional cases (20%), idiopathic RPGN is associated with definite granular immune depos its of IgG and C3, usually in the mesangium and along the subendothelial aspect of the capillary wall [32].…”

Thrombotic Microangiopathy-Kidneys and Beyond: Historic Lessons

“…Deposits of C3, found in glomeruli and arterioles, consistent with the activation of complement and local C3 consumption, and C9 staining in glomeruli and small arteries with intimal proliferation and thrombosis documents activation up to the terminal lytic MAC [19][20][21][22][23][24][25][26]. Same period the role for abnormalities in von Willebrand factor (vWF) metabolism and interaction between platelets and large vWF multimers was suggested in the pathogenesis of HUS/TTP [27][28][29][30].…”