Abstract
The aim of our study was to investigate the expression of kidney injury molecule-1 (KIM-1) in renal allograft biopsy samples and assess the clinical significance of its use as a biomarker for tissue damage. A total of 69 renal allograft biopsy samples from 17 patients with normal serum creatinine and 52 cases of increased serum creatinine were collected. They were divided into different groups according to the Banff 2007 diagnostic criteria. KIM-1 expression was detected by immunohistochemical methods and the association of KIM-1 and blood biochemical indexes was analyzed. KIM-1 expression increased as Banff 2007 classification grade increased and was positively correlated with tubular inflammation severity in the acute T-cell rejection group. Moreover, KIM-1 expression was strongly positive in the chronic active antibody-mediated rejection group. Interestingly, KIM-1 was weakly positive in the normal group without obvious acute rejection and injury of immunosuppressant toxicity. In this group, 27.3% (3/11) of the cases with normal serum creatinine level showed weakly positive KIM-1 expression in their renal tissues. KIM-1 expression level is positively correlated with renal allograft damage and tubular cell injury. KIM-1 is expressed in tubular epithelial cells before blood biochemical indexes become elevated and morphological changes occur. KIM-1 expression is an early, sensitive, and specific biomarker to determine renal tubular epithelial cell injury in renal allograft tissue.
Highlights
Kidney injury molecule- (KIM- ) is a type I transmembrane protein that was first identified in renal cells after injury in [ ]
The results indicated that KIM- expression in renal allograft tissue was positively correlated with declines in kidney function
The results show that KIM- expression in renal allograft tissue is more sensitive than rises in serum creatinine or morphological changes in the assessment of renal tubular epithelial injury
Summary
Kidney injury molecule- (KIM- ) is a type I transmembrane protein that was first identified in renal cells after injury in [ ]. KIM- mRNA and protein are expressed at low levels in normal kidney but are up regulated in dedifferentiated proximal tubular cells after ischemic or nephrotoxic acute kidney injury (AKI). In a kidney biopsy study of patients with CKD from various aetiologies, KIM- was primarily expressed at the luminal side of dedifferentiated proximal tubules, in areas with fibrosis and inflammation [ ]. KIM- staining in the kidney correlated positively with morphological damage and renal function decline. It appears to be a highly sensitive and specific biomarker for the diagnosis of acute or chronic renal injury [ , ]. Our study was designed to explore KIM- expression in renal allograft biopsy and assess the clinical significance of its use as a potential biomarker of renal tissue injury
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