Glomerular expression of kidney injury molecule-1 and podocytopenia in diabetic glomerulopathy. Am J Nephrol 2011;34(3):268-80
Date
08/09/2011Pubmed ID
21822010Pubmed Central ID
PMC3169370DOI
10.1159/000330187Scopus ID
2-s2.0-79961115589 (requires institutional sign-in at Scopus site) 51 CitationsAbstract
BACKGROUND/AIMS: Studies have shown that kidney injury molecule-1 (KIM-1) is upregulated in damaged renal proximal tubules. In this study, we examined KIM-1 expression in glomerular epithelial cells in diabetic glomerulopathy.
METHODS: Renal histology, immunostaining and Western blot for protein level, and real-time PCR for mRNA expression of KIM-1 and podocyte markers were evaluated in untreated or losartan-treated Zucker lean (Fa/+) and Zucker diabetic fatty (Fa/Fa) rats.
RESULTS: The diabetic rats showed an increased glomerular expression of KIM-1. KIM-1 staining was localized primarily in the hyperplastic parietal epithelium of Bowman's capsule in the early stages of diabetes with subsequent increase in KIM-1-positive cells in the glomerular tuft in the more advanced stages. The increase in glomerular KIM-1 was associated with a decrease in podocytes in Fa/Fa rats. Antiproteinuric treatment with losartan attenuated podocytopenia and decreased renal expression of KIM-1 in treated diabetic rats. In an in vitro study, albumin overload increased KIM-1 protein in the primary cultures of rat glomerular epithelial cells.
CONCLUSION: These results show that glomerular KIM-1 expression was increased, in proportion to the extent of proteinuria and podocytopenia in the diabetic animals, supporting that KIM-1 could be used as a potential biomarker for glomerular injury in proteinuric kidney disease.
Author List
Zhao X, Zhang Y, Li L, Mann D, Imig JD, Emmett N, Gibbons G, Jin LMMESH terms used to index this publication - Major topics in bold
AnimalsCell Adhesion Molecules
Cells, Cultured
Diabetic Nephropathies
Epithelial Cells
Kidney Glomerulus
Male
Podocytes
Rats
Rats, Zucker
