Upon vascular injury, newly exposed tissue factor and subendothelial
collagen cause platelet activation and adhesion to the site of injury.
Acute cytomegalovirus infection induces a subendothelial
inflammation (endothelialitis) in the allograft vascular wall.
Interestingly, 100% exhibited membranoproliferative glomerulonephritis, with immunofluorescence demonstrating subendothelial
and intraglomerular deposits of IgG, IgM, and C3.
layer of the intima in arteries and arterioles contains a sheetlike layer or lamella of fenestrated elastic material called the internal elastic membrane.
Half of the rabbits in group, CHOL + CM showed no pathological changes in either the aortae, and in the other half of the animals the changes were limited to slight damages in endothelium and inner layer and small subendothelial
deposits of lipids.
Primary hemostasis is defined as the platelet-vessel wall interaction at the site of vascular injury that initiates when flowing platelets recognize (through their receptors) and bind (through the adhesive protein von Willebrand factor) subendothelial
These clinical manifestations are usually sustained by membranous GN histological pattern, defined by mesangial proliferation and basement membrane thickening at microscope, subendothelial
and mesangial electron-dense deposits made up by IgM, IgG3 and C3 at electron microscopy, suggesting deposition of circulating immune complexes (1-2, 5).
The NO radical readily reacts to form other reactive oxygen and nitrogen species (RONS) capable of producing oxidative damage, destruction of extracellular matrix (ECM) and connective tissue in the subendothelial
Adhesion molecules, such as sICAM-1 and sVCAM-1, have been used as early biomarkers of atherosclerosis because of their participation in the initial step of the disease, in which they promote the translocation of monocytes and leucocytes to the arterial endothelium with subsequent migration to the subendothelial
space, initiating the atherosclerosis process (Chen et al.
This entity includes 3 subtypes: type I MPGN, with subendothelial
deposits, classic-type mesangiocapillary glomerulonephritis; type II MPGN, with dense deposits in the GBMs; and type III MPGN, with mixed membranous and proliferative glomerulonephritis.
The vasculitis involves destruction of small to medium-sized arteries that contain an inflammatory infiltrate within the vessel wall and subendothelial
space, leading to destruction of the elastic lamina (figure 1).
The deficiency of von Willebrand's factor led to a secondary reduction in plasma factor VIII level and impaired platelet adherence to subendothelial