狼疮性肾炎
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免疫学检查
病因与发病机制
临床表现
狼疮性肾炎
病理改变
预后
诊断和治疗
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Factors associated with development of systemiclupus erythematosus
Sunlight
Drugs: >100 described in association with drug induced lupus
Epstein-Barr virus
Abnormalities of apoptosis
Abnormal signal transduction: toll like receptors
Cytokine patterns: interferon signature; decreased interleukin 2 from T cells
Genes: CRP and serum amyloid P genes, FcγR receptors,programmed cell death
Occupational exposure: silica, pesticides, mercury
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LN的发病机制
抗DNA抗体和免疫复合物诱导肾脏损伤
B淋巴细胞产生具有致病性的抗DNA抗体等自身抗体
体内核小体增多或异常核小体出现
辅助性T淋巴细胞参与激活B淋巴细胞
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The glomerular patterns of injury in SLE.
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International society of nephrology/renal pathology society classification of lupus nephritis(2003)
Class Description
Class I
Minimal mesangial lupus nephritis
Normal at light microscopy
Mesangial deposits on immunofluorescence
Class II
Mesangial proliferative lupus nephritis
Mesangial hypercellularity or expansion with mesangial immune deposits
Some subepithelial or subendothelial deposits on immunofluorescence by electron microscopy
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Class III
Focal lupus nephritis
Involves <50% glomeruli. Active or inactive lesions typically with subendothelial deposits
A: Active lesions; focal proliferative lupus nephritis
A/C: Active and chronic lesions; focal proliferative and sclerosing lupus nephritis
C: Chronic inactive lesions with glomerular scars; focal sclerosing lupus nephritis
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Class IV
Diffuse lupus nephritis
Involves >50% glomeruli. Active or inactive diffuse, segmental or global endo- or
extracapillary glomerulonephritis. Typically with subendothelial deposits. Divided into
diffuse segmental (S) when >50% of involved glomeruli have segm
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