Fibrinoid necrosis

Fibrinoid necrosis is a pathological lesion that affects blood vessels, and is characterized by the occurrence of endothelial damage, followed by leakage of plasma proteins, including fibrinogen, from the vessel lumen; these proteins infiltrate and deposit within the vessel walls, where fibrin polymerization subsequently ensues.[1][2][3][4]

Although the term fibrinoid essentially means "fibrin-like", it has been confirmed through immunohistochemical analysis and electron microscopy that the areas referred to as "fibrin-like" do contain fibrin, whose predominant presence contributes to the bright, eosinophilic (pinkish) and structureless appearance of the affected vessels.[4][5][6][7]

The earliest documented identification of fibrinoid changes dates back to 1880, when it was questioned whether these histological changes resulted from the deposition of a fibrinous exudate, or the degeneration and breakdown of collagen fibers.[8][9]

The term fibrinoid was introduced to describe these changes, because distinguishing fibrinoid from hyaline deposits posed a significant challenge, as both exhibit a similar appearance under standard light microscopy.[4][8] This morphological similarity necessitated the use of specialized histological staining techniques, such as phosphotungstic acid hematoxylin and various types of trichrome stains, to facilitate the distinction of fibrinoid material. Because these stains possess the ability to highlight and identify fibrin, this led to the term fibrinoid, which means "fibrin-like", being used to describe the affected vessels.[4]

Nevertheless, as early as 1957, fibrin was indeed identified within fibrinoid, and by 1982, this understanding had advanced, with many researchers recognizing fibrinoid as a complex structure primarily composed of fibrin interwoven with various plasma proteins.[8]

  1. ^ Strayer, DS; Rubin, E; Saffitz, JE; Schiller, AL (2015). Rubin's Pathology: Clinicopathologic Foundations of Medicine (7th ed.). Philadelphia, Penn.: Wolters Kluwer. ISBN 978-1-4511-8390-0.
  2. ^ Miller, MA; Zachary, JF (2017). "Mechanisms and Morphology of Cellular Injury, Adaptation, and Death". Pathologic Basis of Veterinary Disease: 2–43.e19. doi:10.1016/B978-0-323-35775-3.00001-1. ISBN 978-0-323-35775-3. PMC 7171462.
  3. ^ Chen, H; Liu, Y; Wei, L; Wang, H; Zheng, Z; Yan, T; Jia, J; Li, D (11 December 2023). "The effect of fibrinoid necrosis on the clinical features and outcomes of primary IgA nephropathy". BMC Nephrology. 24 (1): 366. doi:10.1186/s12882-023-03419-4. PMC 10712095. PMID 38082385.
  4. ^ a b c d Rosenblum, WI (October 2008). "Fibrinoid necrosis of small brain arteries and arterioles and miliary aneurysms as causes of hypertensive hemorrhage: a critical reappraisal". Acta Neuropathologica. 116 (4): 361–9. doi:10.1007/s00401-008-0416-9. PMID 18642006.
  5. ^ Hano, H; Takagi, I; Nagatsuma, K; Lu, T; Meng, C; Chiba, S (28 January 2007). "An autopsy case showing massive fibrinoid necrosis of the portal tracts of the liver with cholangiographic findings similar to those of primary sclerosing cholangitis". World Journal of Gastroenterology. 13 (4): 639–42. doi:10.3748/wjg.v13.i4.639 (inactive 12 July 2025). PMC 4065992. PMID 17278236.{{cite journal}}: CS1 maint: DOI inactive as of July 2025 (link)
  6. ^ Cite error: The named reference FNEM was invoked but never defined (see the help page).
  7. ^ WIENER, J; SPIRO, D; LATTES, RG (September 1965). "The Cellular Pathology of Experimental Hypertension. II. Arteriolar Hyalinosis and Fibrinoid Change". The American Journal of Pathology. 47 (3): 457–85. PMC 1920447. PMID 14334752.
  8. ^ a b c Bajema, IM; Bruijn, JA (July 2000). "What stuff is this! A historical perspective on fibrinoid necrosis". The Journal of Pathology. 191 (3): 235–8. doi:10.1002/(SICI)1096-9896(0000)9999:9999<N/A::AID-PATH610>3.0.CO;2-I. PMID 10878543.
  9. ^ Scott, GB (June 1968). "Trypan blue and the generalized Shwartzman reaction. The nature and formation of fibrinoid material in the pulmonary arteries". British Journal of Experimental Pathology. 49 (3): 251–6. PMC 2093816. PMID 5665438.


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