Résumé : | SIGNIFICANCE: There is a reduction in corneal nerve fiber density and length in type 2 diabetes mellitus with chronic kidney disease compared with type 2 diabetes mellitus alone; however, this difference does not result in worse ocular surface discomfort or dry eye disease. PURPOSE: This study aimed to determine the clinical impact of corneal nerve loss on ocular surface discomfort and markers of ocular surface homeostasis in people with type 2 diabetes mellitus without chronic kidney disease (T2DM–no CKD) and those with type 2 diabetes mellitus with concurrent chronic kidney disease (T2DM-CKD). METHODS: Participants were classified based on estimated glomerular filtration rates into two groups: T2DM-CKD (n = 27) and T2DM–no CKD (n = 28). RESULTS: There was a significant difference between the T2DM-CKD and T2DM–no CKD groups in corneal nerve fiber density (14.9 ± 8.6 and 21.1 ± 7.1 no./mm2 , respectively; P = .005) and corneal nerve fiber length (10.0 ± 4.6 and 12.3 ± 3.7 mm/mm2 , respectively; P = .04). Fluorescein tear breakup time was significantly reduced in T2DM-CKD compared with T2DM–no CKD (8.1 ± 4.4 and 10.7 ± 3.8 seconds, respectively; P = .01), whereas ocular surface staining was not significantly different (3.5 ± 1.7 and 2.7 ± 2.3 scores, respectively; P = .12). In terms of ocular surface discomfort, there were no significant differences in the ocular discomfort score scores (12.5 ± 11.1 and 13.6 ± 12.1, respectively; P = .81) and Ocular Pain Assessment Survey scores (3.3 ± 5.4 and 4.3 ± 6.1, respectively; P = .37) between the T2DM-CKD and T2DM–no CKD. CONCLUSIONS: The current study demonstrated that corneal nerve loss is greater in T2DM-CKD than in T2DM–no CKD. However, these changes do not impact ocular surface discomfort or markers of ocular surface homeostasis. |