The Pathogenic Role of Fibrin Deposition in the Glomerular Lesions of Toxemia of Pregnancy

Abstract

An immunofluorescent study of renal biopsies from patients with toxemia of pregnancy has been performed. It was found that the glomeruli consistently showed bright staining for fibrin within endothelial cells, as well as occasional deposits along the basement membrane. Gamma globulin was only occasionally demonstrable, generally in the form of irregular deposits along the basement membrane. ß1C was absent and albumin was not seen in glomeruli, except sometimes in the form of droplets within epithelial cells. In biopsies from pregnant patients without toxemia only equivocal staining for fibrin was seen. On the basis of these observations and other evidence discussed, it is proposed that the accumulation of fibrin in glomeruli reflects a prolonged state of intravascular clotting in toxemia and that the arrest in glomeruli of some form of circulating fibrin constitutes the basic pathogenic mechanism of the glomerular damage in this disease.

Glomerular dynamics and morphologic changes in the generalized Shwartzman reaction in postpartum rats.

“…The increased sensitivity to the generalized Shwartzman reaction in postpartum rats was similar to that reported for pregnant rats (5). While the relative hypercoagulation state of pregnancy has been thought to predispose these animals to the generalized Shwartzman reaction (23), these or other predisposing factors have not been evaluated critically in the postpartum period. Nevertheless, an enhanced susceptibility of 10-d postpartum animals to the renal failure of the generalized Shwartzman reaction was apparent from this study.…”

Biochemical changes in endothelial cell monolayers induced by fibrin deposition in vitro.

“…1 " 4 Fibrin deposits have been observed on and under endothelial surfaces, 15 " 7 and these deposits are a common feature of a variety of diseases, including pre-eclampsia 8 and malignant hypertension. 910 Fibrin deposition on endothelial cells (EC) in vivo 8 and in vitro 11 has resulted in the disorganization of the normal endothelial monolayer architecture.…”

“…910 Fibrin deposition on endothelial cells (EC) in vivo 8 and in vitro 11 has resulted in the disorganization of the normal endothelial monolayer architecture. It has been suggested that this disorganized endothelium promotes atherogenesis, since this would expose the subendothelium over an extended period of time resulting in increased platelet adhesion.…”

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

“…Glomerular deposition of fibrinogen without increased AHF standing was also detected in renal tissue from patients with anaphylactoid purpura nephritis and in recurrent macroscopic hematuria with focal glomerulonephritis. Received for publication 20 September 1973 and in revised form 12 December 1973. experimental renal diseases (1)(2)(3)(4)(5)(6)(7)(8)(9)(10). In addition, fibrin degradation products have appeared in the blood and urine of patients with glomerulonephritis and in renal transplant recipients (11,12).…”