The development of progressive tubular atrophy and interstitial fibros
is represents a final common pathway leading to renal insufficiency. M
y laboratory has been investigating several rat models of primary glom
erular disease in an effort to determine cellular and molecular mechan
isms of renal interstitial fibrosis. These models include puromycin am
inonucleoside nephrosis (PAN) [1-6], protein-overload proteinuria [7,
8], passive Heymann nephritis [9, 10], and diet-induced hypercholester
olemia [11]. From a functional perspective, it is likely that the asso
ciated loss of tubules accounts for the decline in renal function. Fou
r recurrent themes are emerging from our studies.