Persistent glomerulonephritis following the haemolytic-uremic syndrome. Immunopathological and morphological studies.
Immunopathological and ultrastructural studies were carried out on kidney biopsies of eight children with a persistent nephropathy (PN) following the haemolytic-uremic syndrome (HUS). Significant amounts of in vivo-bound immunoglobulins and C3 were demonstrated by immunofluorescence methods in the glomeruli of all the cases, with a nodular pattern along the capillary walls. In four cases studied, C1q and C4 were also demonstrated, with an identical distribution. Transmission electron-microscope studies revealed a marked thickening of the glomerular basement membrane, and the existence of an electron-dense material with an intramembranous and subepithelial localization. With the exception of one case, serum complement studies did not present major modifications. Coagulation studies reveal that alterations observed in acute HUS were not present in the PN. Results of the present study suggest that an immune mechanism of glomerular damage operates in the pathogenesis of the PN observed after HUS, leading to a normocomplementemic, chronic glomerulonephritis. Although a hypothetical antigen (or perhaps several antigens) remains to be demonstrated, immunofluorescence and electron-microscope studies suggest the deposition of immune complexes in the renal lesions.
D001323:Autoantibodies; D001485:Basement Membrane / Q000276:immunology; D001780:Blood Coagulation Tests; D002648:Child; D002675:Child, Preschool; D003165:Complement System Proteins / Q000032:analysis; D005921:Glomerulonephritis / Q000209:etiology* / Q000276:immunology / Q000473:pathology; D006463:Hemolytic-Uremic Syndrome / Q000150:complications*; D006801:Humans; D007136:Immunoglobulins / Q000032:analysis; D007668:Kidney / Q000648:ultrastructure; D008854:Microscopy, Electron
D001323:Autoantibodies; D007136:Immunoglobulins; D003165:Complement System Proteins