Affordable Access

A case of renal amyloidosis associated with hepatic adenoma: the pathogenetic role of tumor necrosis factor-alpha.

Authors
  • Shibasaki, T
  • Matsumoto, H
  • Watabe, K
  • Joh, K
  • Nakano, H
  • Matsuda, H
  • Gomi, H
  • Ohno, I
  • Ishimoto, F
  • Sakai, O
Type
Published Article
Journal
Nephron
Publication Date
Jan 01, 1997
Volume
75
Issue
3
Pages
350–353
Identifiers
PMID: 9069459
Source
Medline
License
Unknown

Abstract

We report a case of a 35-year-old man with secondary amyloidosis chiefly involving the kidney and heart. The patient showed severe proteinuria and ischemic heart damage and had hepatic adenoma at the age of 33. Biopsy specimens from the kidney, heart, stomach and rectum showed extensive deposition of amyloid. After the surgical resection of a 300-gram hepatic adenoma, highly elevated c-reactive protein (CRP) levels decreased and the serum amyloid A (SAA) level was completely normalized. Normal liver cells were immunostained with rabbit anti-SAA antibody, but the cells in adenoma tissue and kidney were not. Electron microscopic examination revealed extracellular deposition of amyloid fibrils in the hepatic adenoma and kidney tissue. The concentration of tumor necrosis factor-alpha (TNF-alpha) (312 pg/mg tissue protein) was 7-fold higher in adenoma tissue than in normal liver tissue. Moreover, SAA (2.8 ng/mg tissue protein) was 2-fold higher in normal liver tissue than in adenoma tissue. Since TNF-alpha has been known to induce SAA production in target cells, the present results suggest that the hepatic adenoma produced TNF-alpha, which then caused mainly secondary amyloidosis in the kidney and heart. Currently, 2 years after surgical resection, urinary excretion of protein has been markedly reduced (from 3.5 to 0.8 g/day) and renal and cardiac functions are normal without specific medical treatment.

Report this publication

Statistics

Seen <100 times