Figure 635

Pathogenesis of Schistosoma mansoni glomerulopathy. Note the crucial role of hepatic fibrosis, which 1) induces glomerular hemodynamic changes; 2) permits schis-tosomal antigens to escape into the systemic circulation, subsequently depositing in the glomerular mesangium; and 3) impairs clearance of immunoglobulin A (IgA), which apparently is responsible for progression of the glomerular lesions. IgA synthesis seems to be augmented through B-lympho-cyte switching under the influence of inter-leukin-10, a major factor in late schistosomal lesions [7].

FIGURE 6-36 ( see Color Plate)

Renal amyloidosis in schistosomiasis. A, Schistosomal granuloma (top), three glomeruli with extensive amyloid deposits (bottom), and dense interstitial infiltration and fibrosis in a patient with massive Schistosoma haematobium infection. (Hematoxylin-eosin stain X 75.) B, Amyloid deposition in the mesangium associated with mild mesangial cellular proliferation in a patient with S. mansoni glomerulopathy (African Association of Nephrology class V). (Hematoxylin-eosin stain X 175.) C, Early amyloid deposits seen as green (birefringent) deposits in a glomerulus with considerable mesangial proliferation in a patient with hepatosplenic schistosomiasis. (Congo red stain X 200, examined under polarized light.)

Pathogenesis of schistoma-associated amyloidosis

Interleukin-1,6 Hepatocyte



Pathogenesis of schistoma-associated amyloidosis


Matrix adhesion

AA protein

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