title: Immunohistochemical analysis of transforming growth factor beta-1 in AA and AL renal amyloidosis.
abstract: It has been found that the prognosis of both AA and AL renal amyloidosis is significantly worse in cases in which the renal cortical interstitium exhibits fibrosis at the time of the biopsy than in those in which it is normal. However, the fibrogenic mechanisms operating locally in the kidney are not well understood. Transforming growth factor beta (TGF-P) has been recognized as a key mediator of renal fibrogenesis. Therefore, the present study on AA and AL renal amyloidosis was undertaken to ascertain if potential pathway towards renal tubulointerstitial fibrosis involves TGF-beta and to examine the possible relationship between the immunoexpression of TGF-beta and interstitial alpha-smooth muscle actin (alpha-SMA) expression as well as interstitial infiltrates. The mean values of the immunoexpression of TGF-beta-1, interstitial CD3+ cells, alpha-SMA expression as well as interstitial area were in AA and AL groups significantly increased in comparison with controls. The mean values of the interstitial CD68+ cells were in both AA and AL groups increased in comparison with controls however in AL amyloidosis this difference was not significant. Moreover, all investigated parameters were significantly increased in AA group as compared to AL cases. In both AA and AL groups there were significant positive correlations between immunostaining of TGFbeta-1 and alpha-SMA as well as immunostaining of TGF-beta-1 and interstitial volume. In the AA group, a significant negative correlation existed between immunostaining of TGF-beta-1 and CD 3+ cells. In the AL group, this correlation tended to be negative, how ever it did not reach statistical significance. In both AA and AL groups we did not find significant relationship between TGF-beta-1 and interstitial monocytes/macrophages. In conclusion, our study suggests a role of transforming growth factor beta-1 in interstitial fibrotic changes in renal AA and AL amyloidosis and we hypothesize that myofibroblast pathway may be important in this process.
authors.affiliation: Department of Nephropathology, Medical University of Lódź. hobo@csk.umed.lodz.pl
authors.forename: Marian
authors.initials: M
authors.lastname: Danilewicz
authors.forename: Małgorzata
authors.initials: M
authors.lastname: Wagrowska-Danilewicz
mesh_terms: D000199:Actins / Q000235:genetics / Q000378:metabolism; D000328:Adult; D000682:Amyloid / Q000378:metabolism*; D000686:Amyloidosis / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D001706:Biopsy; D017252:CD3 Complex / Q000378:metabolism; D005260:Female; D005786:Gene Expression Regulation; D006801:Humans; D007150:Immunohistochemistry; D007674:Kidney Diseases / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D007684:Kidney Tubules / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D008297:Male; D008875:Middle Aged; D053773:Transforming Growth Factor beta1 / Q000235:genetics / Q000378:metabolism*
chemical_list: D000199:Actins; D000682:Amyloid; D017252:CD3 Complex; D053773:Transforming Growth Factor beta1