Related Experiment Video
Updated: May 2, 2026

Author Spotlight: Understanding Retinal Vessel Resilience and Disease Progression
Published on: January 12, 2024
HbA1c variability as an independent risk factor for diabetic retinopathy in type 1 diabetes: a German/Austrian
Julia M Hermann1, Hans-Peter Hammes2, Birgit Rami-Merhar3
1Institute of Epidemiology and Medical Biometry, ZIBMT, University of Ulm, Ulm, Germany.
Objective:
This study aimed to analyze the effect of HbA1c variability on the occurrence of diabetic retinopathy in type 1 diabetes patients.
Patients And Methods:
35,891 patients with childhood, adolescent or adult onset of type 1 diabetes from a large multicentre survey, the German/Austrian prospective documentation system (DPV), were analysed. Cox proportional hazard models were used to examine whether intra-individual HbA1c variability expressed as variation coefficient is an independent risk factor for the occurrence of diabetic retinopathy.
Results:
Kaplan-Meier curves stratified by median HbA1c and variation coefficient revealed that retinopathy-free survival probability is lower when both median HbA1c and HbA1c variability are above the 50th percentile. Cox regression models confirmed this finding: After adjustment for age at diabetes onset, gender and median HbA1c, HbA1c variability was independently associated with the occurrence of diabetic retinopathy. Time-covariate interactions used to model non-proportionality indicated an effect decreasing with duration of diabetes for both median HbA1c and HbA1c variability. Predictive accuracy increased significantly when adding HbA1c variability to the Cox regression model.
Conclusions:
In patients with type 1 diabetes, HbA1c variability adds to the risk of diabetic retinopathy independently of average metabolic control.
Related Concept Videos
Diabetic Retinopathy
Diabetes Mellitus: Type 2 and Gestational
Type II Diabetes Mellitus III: Clinical Manifestations and Diagnosis
Hyperglycemia
Diabetes: Symptoms, Diagnosis, and Complications
Type I Diabetes II: Pathophysiology

