SIGNIFICANCEThere 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.PURPOSEThis 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).METHODSParticipants were classified based on estimated glomerular filtration rates into two groups: T2DM-CKD (n = 27) and T2DM–no CKD (n = 28).RESULTSThere 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.CONCLUSIONSThe 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.