Obstructive nephropathy is one of the most important causes of renal failur
e in infants and children, while polycystic kidney disease (PKD) is a major
cause of renal failure in the adult population. This review summarizes the
evidence that there may be a number of mechanisms common to the pathophysi
ology of both conditions. In animal models of obstructive nephropathy and P
KD, the renal tubular expression of epidermal growth Factor is suppressed,
and expression of clusterin is increased, both of which suggest arrested ma
turation or dedifferentiation of the tubular cell. There is a marked increa
se in apoptosis of epithelial cells in dilated tubules, associated with an
increase in apoptotic stimuli. The renin-angiotensin system is activated in
both obstructive nephropathy and PKD, which may contribute to tubular atro
phy and interstitial fibrosis, which characterize the progression of both c
onditions. Focal cystic dilatation of the tubule is found in obstructive ne
phropathy, while tubular obstruction is present in cystic kidney disease. I
t is therefore likely that elucidation of the effects of mechanical stretch
on renal tubular epithelial cells will contribute to our understanding of
both conditions. Copyright (C) 2000 S. Karger AG, Basel.