A CASE OF RENAL AMYLOIDOSIS ASSOCIATED WITH HEPATIC ADENOMA - THE PATHOGENETIC ROLE OF TUMOR-NECROSIS-FACTOR-ALPHA

We report a case of a 35-year-old man with secondary amyloidosis chief ly involving the kidney and heart. The patient showed severe proteinur ia and ischemic heart damage and had hepatic adenoma at the age of 33. Biopsy specimens from the kidney, heart, stomach and rectum showed ex tensive deposition of amyloid. After the surgical resection of a 300-g ram hepatic adenoma, highly elevated c-reactive protein (CRP) levels d ecreased 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 microsc opic examination revealed extracellular deposition of amyloid fibrils in the hepatic adenoma and kidney tissue. The concentration of tumor n ecrosis 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 tha n in adenoma tissue. Since TNF-alpha has been known to induce SAA prod uction in target cells, the present results suggest that the hepatic a denoma produced TNF-alpha, which then caused mainly secondary amyloido sis in the kidney and heart. Currently, 2 years after surgical resecti on, urinary excretion of protein has been markedly reduced (from 3.5 t o 0.8 g/day) and renal and cardiac functions are normal without specif ic medical treatment.