It is generally accepted that the progressive loss of kidney function resul
ts from a pathogenic process that is independent of the original etiology,
functioning as a final common pathway. Part of this response is characteriz
ed by triggering of interstitial infiltration and induction of tubular dama
ge, As a consequence, tubular epithelial cells (TEC) can become activated a
nd begin to express several inflammatory mediators. In the present review,
we will summarize the potential role of TEC in progressive renal disease, M
uch emphasis will be put on studies using in vitro cultured TEC, These stud
ies have provided more insight into the different signals involved in the r
egulation of the production of inflammatory mediators like complement, cyto
kines and chemokines, as well as progression factors like growth factors an
d matrix component by TEC.