Publication: Diabetic nephropathy: The central role of
renal proximal tubular cells in tubulointerstitial injury
Authors
Phillips, A.O. ; Steadman, R.
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Publisher
Murcia : F. Hernández
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DOI
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info:eu-repo/semantics/article
Description
Abstract
Diabetic nephropathy is now the commonest
cause of end stage renal disease and accounts for 30-
40% of all patients requiring renal replacement therapy.
Furthermore, the incidence of diabetic nephropathy
continues to increase, in part due to the improved
survival of type 2 diabetic patients as the cardiovascular
mortality in this group declines (Ritz and Stefanski,
1996). Clinically incipient nephropathy is first manifest
by the onset of persistent microalbuminuria, after which,
overt diabetic nephropathy is heralded by the appearance
of persistent proteinuria. Subsequently, there is a
progressive decline in glomerular filtration rate (GFR)
resulting, within 5 years, in end stage renal disease in
50% of patients (Hasslacher et al., 1989). The pathology
of the renal lesions are similar in type I and II diabetes
( Taft et al., 1994), although it has been suggested that
there is more heterogeneity in type II diabetes (Chihara
et al., 1986). Studies analysing structural-functional
relationships have demonstrated that the development of
proteinuria correlates with the degree of mesangial
expansion (Mauer et al., 1984; White and Bilous, 2000).
Although diabetic nephropathy was traditionally
considered a primarily glomerular disease, it is now
widely accepted that the rate of deterioration of function
correlates best with the degree of renal tubulointerstitial
fibrosis (Mauer et al., 1984, Bohle et al., 1991). This
suggests that although in the majority of patients the
primary event is a condition manifest by glomerular
changes resulting in proteinuria, the long-term outcome
is determined by events in the renal interstitium. Wi t h
the increasing awareness of the importance of these
pathological interstitial changes, interest has focused on
the role of cells, such as the epithelial cells of the
proximal tubule (PTC) or the interstitial myofibroblast,
in the initiation of fibrosis. The aim of the present
review is to analyse the available data supporting the
role for the PTC in orchestrating renal interstitial fibrosis
in diabetic nephropathy as a result of glucose-dependent
alterations in PTC function. The potential for subsequent e ffects on PTC-fibroblast cross-talk will also be
considered.
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