Loss of tubular cell adhesion may be important in the pathophysiology
of injury to renal tubular cell epithelium. In-vitro model systems hav
e been utilized to examine altered cell adhesion in response to hypoxi
c/anoxic and oxidant-induced cell injury. Alterations in cell cytoskel
eton and cell surface adhesion molecules, including L-CAM and integrin
s, have been demonstrated in these systems, and are probably important
in the pathogenesis of altered structure and function in response to
injury in renal tubular epithelium.