@entity631 associated with industrial XXXX exposure. Study of pathogenetic mechanisms.

@entity1 @entity644 @entity8 @entity35 @entity4295 @entity349 @entity4259 @entity75 @entity229 @entity134 @entity1985 @entity631
The nephrotoxicity associated with @entity349 may be manifested as either @entity4295 or an immune complex @entity631 , depending upon the conditions under which the @entity1 is exposed to the metal. Two @entity1 with industrial exposure to @entity349 developed the @entity1985 due to @entity631 . A multidisciplinary approach was used to define more precisely the pathogenetic mechanisms involved in the production of the @entity8 . Although glomeruli were normal by light microscopy, immunohistochemical studies demonstrated confluent finely granular epimembranous deposits of IgG and C3. This distribution was confirmed at the ultrastructural level with immunoelectron microscopy. High resolution elemental analysis of electron dense inclusions in tubular epithelial phagolysosomes demonstrated energy dispersion spectra characteristic of coexisting @entity349 and @entity4259 . Eluates from the biopsy material were not immunoreactive against normal @entity35 or @entity1 kidney. There was no immunoreactivity of epimembranous deposits with antibodies having renal tubular epithelial antigen or urinary uromucoid specificity. These observations suggest that a distinctive @entity75 is associated with @entity349 -associated membraneous @entity631 , that the role of the metal itself may only be coincidental, and that the involved antigen remains unknown. @entity229 therapy had no documented persistent beneficial influence upon the level of @entity644 in one @entity1 who has been lost to follow-up. In one @entity1 not treated with @entity134 therapy, withdrawal of exposure to the metal resulted in disappearance of @entity349 from body fluids and clinical remission.
