Diabetic nephropathy is one of the leading causes of renal failure in Weste
rn countries, where diabetic patients account for nearly half of all patien
ts on haemodialysis. Progressive expansion of the mesangial matrix, and thi
ckening of the glomerular and tubular basement membranes without signs of m
ajor cell proliferation are hallmarks of human and experimental diabetic ne
phropathy. These lesions eventually lead to glomerular fibrosis, a central
pathological feature in many human acute and chronic kidney diseases, which
progressively destroys the renal filtration unit, and may finally cause re
nal failure. Indeed, structure-function relationship studies have shown tha
t mesangial matrix expansion is strongly related to the clinical manifestat
ion of diabetic nephropathy.