Fibrinoid necrosis is a form of necrosis, or tissue death, in which there is accumulation of amorphous, basic, proteinaceous material in the tissue matrix with a staining pattern reminiscent of fibrin. It is associated with conditions such as immune vasculitis (e.g. Henoch-Schönlein purpura), malignant hypertension, or hyperacute transplant rejection.
Fibrinoid material does usually contain fibrin and tends to be eosinophilic (staining red with the acidic dye eosin). However, in systemic lupus erythematosus the fibrinoid deposits may contain significant amounts of nuclear debris, including acidic DNA, and may be haematoxyphilic (staining purple or blue with the basic dye haematoxylin). Fibrinoid necrosis is distinguished from hyaline deposits, which are more homogeneous and glassy, and caseous necrosis, which is associated with the tuberculosis. Fibrinoid is now a somewhat historic term, based on traditional haematoxylin and eosin staining. Its significance is different in different contexts, such as malignant hypertension and rheumatoid nodules. However, in context it remains a diagnostically useful term. The idea that autoimmune diseases such as systemic lupus and rheumatoid arthritis were based on a common lesion of 'fibrinoid necrosis of collagen' led to the popular term 'collagen vascular disease', which is now obsolete. It is cells that are dead, not collagen. The presence of fibrin indicates that nearby blood vessels have become highly permeable and often themselves destroyed but vasculitis is not necessarily present at sites of fibrinoid deposition.
Fibrinoid necrosis can be associated with immune-complex associated disease, as in the synovitis and nodules of rheumatoid arthritis and various forms of immune- based vasculitis and glomerular disease. It may be associated with deposition of immune complexes and complement components in vessel walls. In small vessel vasculitis fibrin plugs frequently occur in the vessel lumen, but the term fibrinoid is usually used to refer to material outside the lumen of a vessel.[1]Fibrinoid necrosis also occurs in the walls of arterioles in malignant hypertension (blood pressure greater than 200/130 mmHg).[2]
Fibrinoid necrosis involves the deposition of immune complexes in areas such as the glomerulus and capillaries. The immune complexes do not cause the damage, but activate the alternative complement pathway, specifically C5a, which attracts neutrophils. The neutrophils are then responsible for causing fibrinoid necrosis.