Biological Variation in HbA1c Predicts Risk of Retinopathy and Nephropathy in Type 1 Diabetes
Response to McCarter et al.
- Saul Genuth, MD12,
- John M. Lachin, SCD3 and
- David M. Nathan, MD4
- 1Division of Clinical and Molecular Endocrinology, Case Western Reserve University, Cleveland, Ohio
- 2Division of Endocrinology, University Hospitals of Cleveland, Cleveland, Ohio
- 3Department of Biostatistics and Epidemiology, George Washington University, Washington, D.C
- 4Department of Medicine, Harvard Medical School, Boston, Massachusetts
- Address correspondence to Saul Genuth, MD, Room 430, Biomedical Research Building, Case Western Reserve University, 10900 Euclid Ave., Cleveland, OH 44106-4951. E-mail: smg15{at}cwru.edu
McCarter et al. (1) report that the propensity to glycate hemoglobin, as evidenced by a higher-than-expected HbA1c level for the concomitantly measured mean blood glucose (MBG) level, is itself a risk factor for diabetic retinopathy and nephropathy. They use publicly available data from the Diabetes Control and Complications Trial (DCCT) to calculate a hemoglobin glycation index (HGI) to support their hypothesis. Their results appear to offer a possible explanation for anecdotal reports that some patients with chronically excellent control are nonetheless severely affected by diabetic retinopathy and/or nephropathy, while others with chronically poor glycemic control nonetheless escape these complications.
The data from the National Institute of Diabetes and Digestive and Kidney Diseases–funded DCCT were placed in the public domain to allow other investigators to pursue additional analyses, and we applaud their efforts. However, we the principal investigators of the DCCT cannot accept …
