title: [Participation of apoptosis in renal amyloidosis].
abstract: Renal amyloidosis shows symptoms of renal dysfunction due to the deposition of amyloid protein in the kidney. Recently, it was reported that apoptosis plays an important role in the pathogenesis of type-2 diabetes mellitus and Alzheimer's disease of which amyloid deposition is seen in the tissue. We investigated whether or not apoptosis and related factors are observed in renal amyloidosis. In situ nick end labeling (TUNEL) was performed in seven autopsied renal tissues with primary and secondary amyloidosis and 10 autopsied renal tissues without renal disease as the control. The number of TUNEL-positive cells was significantly increased in both the glomeruli and tubulus of the kidney with amyloidosis than in the control. Electron microscopic analysis was performed on one biopsied renal tissue with amyloidosis and six biopsied renal tissues with minor abnormalities as the control. Typical apoptotic cells were observed only in the former. Bax product, an inducer of apoptosis, and Bcl-2 protein, an inhibitor of apoptosis, were examined immunohistochemically in the seven autopsied renal tissues with amyloidosis and 10 autopsied control tissues. Bax was overexpressed in the tubulus and glomeruli of subjects with renal amyloidosis, compared to the normal controls. However, Bcl-2 protein was not detected in the glomeruli in any of the subjects examined. These results indicate that apoptotic cells are increased in number in renal amyloidosis and Bax overexpression may play an important role in this increase.
authors.affiliation: Second Department of Medicine, Gifu University School of Medicine, Japan.
authors.forename: J
authors.initials: J
authors.lastname: Hiraoka
authors.forename: K
authors.initials: K
authors.lastname: Asano
authors.forename: H
authors.initials: H
authors.lastname: Sano
authors.forename: K
authors.initials: K
authors.lastname: Fujisawa
authors.forename: M
authors.initials: M
authors.lastname: Ohno
authors.forename: G
authors.initials: G
authors.lastname: Takemura
authors.forename: S
authors.initials: S
authors.lastname: Minatoguchi
authors.forename: H
authors.initials: H
authors.lastname: Ohashi
authors.forename: T
authors.initials: T
authors.lastname: Fujiwara
authors.forename: H
authors.initials: H
authors.lastname: Fujiwara
mesh_terms: D000368:Aged; D000686:Amyloidosis / Q000175:diagnosis / Q000209:etiology*; D017209:Apoptosis / Q000502:physiology*; D015415:Biomarkers / Q000032:analysis; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D007668:Kidney / Q000473:pathology / Q000648:ultrastructure; D007674:Kidney Diseases / Q000175:diagnosis / Q000209:etiology*; D008297:Male; D008854:Microscopy, Electron; D008875:Middle Aged; D011518:Proto-Oncogene Proteins / Q000032:analysis; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000032:analysis; D000685:Serum Amyloid A Protein / Q000032:analysis; D051028:bcl-2-Associated X Protein
chemical_list: C494826:BAX protein, human; D015415:Biomarkers; D011518:Proto-Oncogene Proteins; D019253:Proto-Oncogene Proteins c-bcl-2; D000685:Serum Amyloid A Protein; D051028:bcl-2-Associated X Protein