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2012年9月26日星期三

IgA nephropathy IgAN

IgA nephropathy (IgA nephropathy IgAN) Also known as Berger disease glomerular mesangial IgA or IgA deposition with or not associated with other immunoglobulin deposition in the mesangial area of ​​primary glomerular disease clinical manifestations: recurrent episodes of gross hematuria or microscopic hematuria may be associated with varying degrees of proteinuria in some patients severe hypertension or renal insufficiency. Classification of Diseases Primary IgA nephropathy: common disease caused by the kidney itself Secondary IgA nephropathy: caused by diseases other than kidney: of purpura nephritis HIV infection seronegative spondyloarthritis tumor leprosy liver disease familial IgA nephropathy [] Causes The exact pathogenesis of IgA nephropathy is not yet entirely clear that a variety of factors and the incidence of views about the relatively consistent IgAN glomerular disease caused by the case of immune complexes Relationship with the immune system: IgA nephropathy in multimeric IgA (PIgA) show that in the glomerular deposition of IgA immune system leads to the deposition of the circulatory system of the PIgA molecules and mesangial area Relationship with the bone marrow: glomerular mesangial deposits of IgA and present in the blood of IgA similar hinge region glycosylation abnormalities suggest that patients with IgA nephropathy IgA deposition in glomerular mesangial area of ​​bone marrow-derived IgA Relationship with cytokines: patients with IgA nephropathy mesangial area of ​​IgA deposition caused mesangial cells secrete inflammatory cytokines [] [] Pathophysiological The IgA nephropathy iconic pathological changes in IgA deposition in glomerular mesangial area in most patients with concomitant CIgG IgM deposition LEE classification: Level I: glomerular lesions: the vast majority of normal occasional mild mesangial widening (segments) with or without cell proliferation; the tubulointerstitial changed: normal Grade Ⅱ: glomerular lesions: glomerular focal mesangial proliferation and sclerosis (%) rare small crescent; tubulointerstitial change: Grade Ⅲ: glomerular lesions: diffuse mesangial proliferation and widened (occasionally focal stage) and occasionally small crescent balloon adhesions; the tubulointerstitial changes to: Board Zaojian interstitial edema occasionally the cell infiltration rare tubular atrophy Ⅳ: glomerular lesions: severe diffuse mesangial proliferation accompanied by hardening of some or all of glomerulosclerosis visible crescent (<%); tubulointerstitial change: tubular atrophy, interstitial infiltration occasionally interstitial foam cells Ⅴ grade: glomerular lesions: lesions similar Ⅳ level, but more serious visible crescent (%); tubulointerstitial change: similar Ⅳ grade but more serious

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