Concordance of retinopathy and nephropathy over time in Type 1 diabetes: an analysis of data from the Diabetes Control and Complications Trial

Abstract

Aims: Little is known about the dynamic relationship over time between diabetic retinopathy and nephropathy. Thus, we sought to evaluate the concordance over time of retinopathy and nephropathy in patients with Type 1 diabetes during the Diabetes Control and Complications Trial.

Methods: This analysis was conducted in patients with Type 1 diabetes participating in the Diabetes Control and Complications Trial. Only participants with urinary albumin excretion rate < 40 mg/24 h were included in the analysis (n = 1365). We evaluated the relationship between the progression of retinopathy and the development of nephropathy over a mean 6.5 years of follow-up. Progression of retinopathy was defined by 3-step change in Early Treatment Diabetic Retinopathy Study score on consecutive annual evaluations. Development of nephropathy was defined as incidence of urinary albumin excretion rate ≥ 40 mg/24 h on annual evaluation.

Results: Over a mean 6.5 years of follow-up, the incidence of progression of retinopathy was higher in those who developed nephropathy than in those who did not (36.2 vs. 13.4%; P < 0.001). The development of nephropathy independently increased the risk for progression of retinopathy (hazard ratio 1.62, 95% CI 1.23-2.13, P = 0.001), after adjustment for age, gender, diabetes duration, treatment, HbA1c , BMI, HDL cholesterol and blood pressure. Similarly, the incidence of nephropathy was higher in participants who had progression of retinopathy than in those who did not (40.7 vs. 15.7%; P < 0.001). Furthermore, progression of retinopathy independently increased the risk for development of nephropathy (hazard ratio 1.72, 95% CI 1.30-2.27, P < 0.001).

Conclusions: Progression of retinopathy and development of nephropathy each increase the risk for incidence of the other, independent of established risk factors for microvascular complications, supporting the notion of a shared aetiologic basis.