Glomerular expression of kidney injury molecule-1 and podocytopenia in diabetic glomerulopathy.

Abstract:

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.

journal_name

Am J Nephrol

authors

Zhao X,Zhang Y,Li L,Mann D,Imig JD,Emmett N,Gibbons G,Jin LM

doi

10.1159/000330187

subject

Has Abstract

pub_date

2011-01-01 00:00:00

pages

268-80

issue

3

eissn

0250-8095

issn

1421-9670

pii

000330187

journal_volume

34

pub_type

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