Since urinary shear stress is most likely modified in chronic kidney diseases (mainly because of variations of urinary flow observed in obstructive, diabetic or hypertensive nephropathies and after renal mass reduction), we hypothesize that changes in urinary shear stress potentially contribute to the progression of renal disease.
We study the response of renal tubular cells to shear stress using a home-made device (picture) which allows both short- and long term in vitro exposure of cultured cells to continuous and well controlled shear stress under laminar flow conditions.
Results demonstrated that renal tubular cells lose an important number of their epithelial characteristics (tight junctions, adherens junctions, primary cilium) and upregulate tubular damage markers (Kim1, Ngal) after exposure to shear stress (Miravète et al 2012, Maggiorani, Dissard et al, 2015). In addition, shear stress-submitted cells secrete mediators that stimulate adhesion of monocytes to endothelial cells and their differentiation into inflammatory macrophages (Miravète et al 2011, 2012).
Thus, changes in urinary shear stress should be considered as potential insults for tubular cells leading to both disorganization of the tubular epithelium and renal inflammation, two key events in the progression of nephropathies. Further studies on the mechanisms associated to urinary shear stress-induced alterations would be now of great interest to propose new targets to slow-down progression of chronic kidney disease.