Advanced Glycation End Products and Receptors in Fuchs’ Dystrophy Corneas Undergoing Descemet’s Stripping with Endothelial Keratoplasty

PurposeTo describe the histopathologic features of Descemet’s membrane (DM) obtained from Fuchs’ endothelial corneal dystrophy (FECD) corneas undergoing Descemet’s stripping with endothelial keratoplasty (DSEK) and to assess the presence of advanced glycation end products (AGEs) and their receptors in FECD endothelium and DM.DesignProspective observational case series.ParticipantsFive eyes of 5 patients undergoing DSEK for FECD and 4 normal control eyebank corneas.MethodsDescemet’s membrane and corneal endothelium from FECD patients undergoing DSEK were assessed with hematoxylin–eosin staining and immunohistochemistry for AGEs, receptor of AGEs (RAGE), and galectin 3 (AGE-R3).Main Outcome MeasuresHistopathologic abnormalities and presence of AGEs, RAGE, and AGE-R3 in DSEK specimens.ResultsHistopathologic assessment of DSEK specimens from FECD patients disclosed thickening and nodularity of DM and loss of endothelial cells. Immunohistochemical staining of FECD DM for AGE, RAGE, and AGE-R3 showed an abundance of AGEs in the anterior portion of DM, mild positivity for RAGE, and moderate positivity for AGE-R3.ConclusionsTissue quality after DSEK is sufficient to allow detailed histopathologic analysis. The presence of AGEs, RAGE, and AGE-R3 in DM and corneal endothelium of FECD patients supports a link between accumulation of AGEs, oxidative stress, and corneal endothelial cell apoptosis in the pathogenesis of FECD.