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1 Renal Unit and Department of Medicine, Massachusetts General Hospital, Charlestown 02129; 2 Section of Nephrology, Yale University School of Medicine, New Haven, Connecticut 06519; and 3 Harvard-Massachusetts Institute of Technology, Division of Health Sciences and Technology, Cambridge, Massachusetts 02139
Kidney injury molecule-1 (Kim-1) is a
type 1 membrane protein maximally upregulated in proliferating and
dedifferentiated tubular cells after renal ischemia.
Because epithelial dedifferentiation, proliferation, and local
ischemia may play a role in the pathophysiology of autosomal
dominant polycystic kidney disease, we investigated Kim-1 expression in
a mouse model of this disease. In the Pkd2WS25/
mouse
model for autosomal dominant polycystic kidney disease, cystic kidneys
show markedly upregulated Kim-1 levels compared with noncystic control
kidneys. Kim-1 is present in a subset of cysts of different sizes and
segmental origins and in clusters of proximal tubules near cysts.
Kim-1-expressing tubular cells show decreased complexity and quantity
of basolateral staining for Na-K-ATPase. Other changes in polarity
characteristic of ischemic injury are not present in
Kim-1-expressing pericystic tubules. Polycystin-2 expression is
preserved in Kim-1-expressing tubules. The interstitium surrounding
Kim-1-expressing tubules shows high proliferative activity and staining
for smooth muscle 
-actin, characteristic of myofibroblasts. Although
the functional role of the protein in cysts remains unknown, Kim-1
expression in tubules is strongly associated with partial
dedifferentiation of epithelial cells and may play a role in the
development of interstitial fibrosis.
Na-K-ATPase; cell polarity; fibrosis; Tim; ischemia; kidney obstruction
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