Related Experiment Videos
Glomerular alterations associated with obstructive jaundice
1Department of Pathology, Tokyo Metropolitan Komagome Hospital, Japan.
An immunohistochemical and clinicopathologic analysis of glomerular alterations was carried out in 20 autopsy cases with obstructive jaundice. The 20 cases without clinical nephritis had primary carcinoma of various locations, including the stomach, rectum, pancreas, and biliary tract. Mesangial IgA deposition was present on immunofluorescence staining in four cases, IgG in two cases, IgM in five cases, and C3 in four cases. Glomerular polymeric IgA containing A1, A2, and J chain was considered to originate from the gastrointestinal tract. All immunofluorescence-positive cases except one had electron-dense deposits in mesangial regions. These findings suggest that glomerular IgA deposition develops in a handful of patients suffering from obstructive jaundice, presumably due to the passive trapping of circulating immune complexes. Furthermore, glomerular IgA deposition in patients with obstructive jaundice is not influenced by duration or intensity of jaundice, and it unlikely induces clinical nephritis.
An immunohistochemical and clinicopathologic analysis of glomerular alterations was carried out in 20 autopsy cases with obstructive jaundice. The 20 cases without clinical nephritis had primary carcinoma of various locations, including the stomach, rectum, pancreas, and biliary tract. Mesangial IgA deposition was present on immunofluorescence staining in four cases, IgG in two cases, IgM in five cases, and C3 in four cases. Glomerular polymeric IgA containing A1, A2, and J chain was considered to originate from the gastrointestinal tract. All immunofluorescence-positive cases except one had electron-dense deposits in mesangial regions. These findings suggest that glomerular IgA deposition develops in a handful of patients suffering from obstructive jaundice, presumably due to the passive trapping of circulating immune complexes. Furthermore, glomerular IgA deposition in patients with obstructive jaundice is not influenced by duration or intensity of jaundice, and it unlikely induces clinical nephritis.