Morphologic contribution on gross hematuria in mild mesangioproliferative glomerulonephritis without crescents.

Abstract

In order to clarify the pathogenesis of gross hematuria in mild forms of mesangioproliferative glomerulonephritis without crescents, systematic light microscopic, immunohistologic, electron microscopic, and some scanning electron microscopic investigations were carried out on 17 cases of this disease, in part on serial sections. The investigations produced the following results: In gross hematuria, erythrocytes pass into Bowman's space in the area of basement membrane ruptures. The basement membrane ruptures occur at sites where the basement membrane is infiltrated in its entire width by aggregated immune complexes. This occurs when these immune complexes are detached from the basement membrane by lysosomal digestion. As a working hypothesis, it is furthermore considered possible that in diseases accompanied by increased IgA production, circulating IgA is deposited at a higher rate in the glomerular filtration barrier and it is there degraded by an excessive reaction of local cells before morphologically identifiable immune complexes appear. In this process the basement membrane undergoes local destruction. It is also assumed that in gross hematuria, immune complexes other than IgA or hitherto unknown substances enter the basement membrane during the filtration process and trigger frustrane phagocytosis at the basement membrane by their presence, with consecutive basement membrane destruction. It is pointed out that gross hematuria occurs most often in mild forms of mesangioproliferative glomerulonephritis with IgA and C3 deposits in the mesangium and sometimes also in the capillary periphery. It could be shown that in mild forms of mesangioproliferative glomerulonephritis, hematuria occurs more often in the male sex.(ABSTRACT TRUNCATED AT 250 WORDS)