Pathology of lupus nephritis

1 pathogenesis
Pathogenesis of lupus nephritis there is no affirmative, can be replicated, animal experiments and clinical results are consistent conclusion. At present, most scholars believe that some foreign antigen (eg, retrovirus) and endogenous antigen (such as DNA immunization needed protein, lymphocyte surface antigen) role in immune regulation dysfunction in patients with highly active proliferation of B lymphocytes to produce a large number of autoantibodies, and combined with the corresponding antigen to form immune complex deposition in the glomerulus is the main pathogenesis of lupus nephritis. DNA and glomerular basement membrane binding, and the cycle of anti-DNA antibodies in situ formation of immune complexes can also be involved in lupus nephritis. Complement component defects in red blood cells and phagocytosis of FC or C3b receptor density on the cell to reduce the clearance of immune complexes decreased ability to increase immune complex deposition in the tissues, increased tissue damage. Complement activation, chemokine formation, leukocyte aggregation, and then released a series of inflammatory mediators and cytokines, leading to inflammation and glomerular damage of small blood vessels. At the same time, the renal interstitial obvious leukocyte and macrophage infiltration, with intercellular adhesion molecule (ICAM) and MHC antigen.The severity of renal interstitial lesion is usually associated with glomerular lesions.Some patients mild glomerular lesions, mainly interstitial vascular disease.
(2) pathological changes
Due to the complexity of the pathogenesis of lupus nephritis, renal pathological changes also showed the diversity and varied, each patient's glomerular, tubulointerstitial and small blood vessels may appear different changes. Lupus nephritis histological changes in glomerular, tubulointerstitial and vascular changes also determine the prognosis of patients. Renal histopathological damage, depends largely on the number of antibody deposition and the intensity of the inflammatory response induced. Persistent antibody deposition, and continue to cause inflammation, eventually leading to irreversible damage. Pathological changes characterized by: wire ring lesions: electron microscopy and immunofluorescence under the sediments of a large number of endothelial endothelial sediment leaving the basement membrane thickening, is an important feature of lupus nephritis kidney damage; Hematoxylin bodies: the general anti-nuclear body in place to cause cell damage caused by the nuclear chromatin gathered together; necrotizing vasculitis: the arterioles and capillaries were cellulose necrosis; electron microscope, electron dense deposits, nuclear fragmentation, virus-like particles and inclusions; immunofluorescence: diffuse granular sediments, mainly IgG, C3.