Elevated plasma TGF-beta 1 in renal diseases: Cause or consequence?

Citation
U. Junker et al., Elevated plasma TGF-beta 1 in renal diseases: Cause or consequence?, CYTOKINE, 12(7), 2000, pp. 1084-1091
Citations number
21
Categorie Soggetti
Cell & Developmental Biology
Journal title
CYTOKINE
ISSN journal
10434666 → ACNP
Volume
12
Issue
7
Year of publication
2000
Pages
1084 - 1091
Database
ISI
SICI code
1043-4666(200007)12:7<1084:EPT1IR>2.0.ZU;2-3
Abstract
We previously reported elevated levels els of TGF-beta 1 in patients,vith r enal carcinoma, Certain aspects led us to ask whether they might be caused by chronic damage to the kidney(s). Here we report on an extended set of pa tients,vith various renal diseases, lung cancer, humoral immunodeficiency a nd controls. For latent TGF-beta 1 in plasma, we find that the control, imm unodeficiency;, lung cancer and kidney transplant groups do not differ sign ificantly (means, 7.0-8.8 ng/ml), Also, acute short-term renal stress (extr acorporal lithotrypsy) does not lead to an increase of TGF-beta 1. However, the pyelonephritis patients present with levels of 19.0 ng/ml, chronic ext racorporal dialysis patients with 15.5 ng/ml, and renal cell carcinoma pati ents with 22.8 ng/ml, For active TGF-beta 1 these findings are exactly reco vered, For serum levels, only the renal carcinoma group presents with signi ficantly elevated levels of TGF-beta 1, Kidney transplantation seems to nor malize TGF-beta 1 levels, while in the kidney cancer patients surgery has a n effect only in part of the group. We conclude that elevated plasma TGF-be ta 1 levels are common in at least two chronic renal disease conditions, an d that it normalizes with restoration of renal function. It is tempting to speculate that chronic elevation of TCF-beta 1 in these patients may be cri tically involved in these conditions predisposing to renal cancer, (C) 2000 Academic Press.