To identify risk factors for diabetic retinopathy in insulin-dependent diabetes mellitus (IDDM), we studied the relationships among residual β-cell function, human leukocyte antigen (HLA), long-term glycemic control, and development of diabetic retinopathy in 128 IDDM patients. Residual β-cell function was assessed by serum C-peptide immunoreactivity (CPR) response to a 100-g oral glucose load (ΔCPR). The patients were stratified into three groups: those with ΔCPR of <0.033 nmol/1 (group 1, n = 50), those with ΔCPR of 0.033–0.1 nmol/1 (group 2, n = 38), and those with ΔCPR of > 0.1 nmol/1 (group 3, n = 40). The cumulative incidence rate of background retinopathy was higher in the order of groups 1, 2, and 3 (P = 0.032). Group 1 progressed to preproliferative retinopathy at an earlier stage than did groups 2 and 3 combined (P = 0.028). Further progression to proliferative retinopathy tended to be earlier in group 1 than in groups 2 and 3 combined (P = 0.083). The mean HbA1c value rose from 9.01 ± 1.06% (mean ± SD) in group 3 to 9.75 ± 0.79% in group 2 to 10.48 ± 1.12% in group 1 (P <0.0001). In group 1, 89.6% of the patients had HLA-A24, whereas 50 and 43.6% of the patients had this antigen in groups 2 and 3 respectively (P <0.0001). In Cox's proportional hazards model, both serum CPR response and mean HbA1c value were identified as independent risk factors for development of diabetic retinopathy after adjusting for other potential risk factors. These results indicate that complete loss of β-cell function, which is associated with HLA-A24, predicts earlier occurrence of diabetic retinopathy through metabolic control.

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