Severe retinopathy in type 1 diabetic patients is not related to the levelof plasma homocysteine

The vascular-injuring amino acid homocysteine was previously shown to be in creased in plasma in type 1 diabetic patients with clinical signs of nephro pathy. Previous studies have also shown an inconsistent relationship betwee n the development of diabetic nephropathy and retinopathy, indicating diffe rent pathogenetic mechanisms. In this study, plasma homocysteine was measur ed in 25 type 1 diabetic patients with a well-characterized form of severe retinopathy. Furthermore, a group of 24 type 1 diabetic patients with simil ar age at onset of diabetes and diabetes duration with no or minimal backgr ound retinopathy were investigated, in order to determine whether plasma ho mocysteine levels are different from those in patients with severe retinopa thy. Patients with severe retinopathy did not have higher plasma levels of homocysteine (13.9 mu moI/L; 5.9-30.7, median and range) than those without retinopathy (10.4 mu mol/L; 5.7-18.9). Within the group of patients with s evere retinopathy, increased homocysteine levels were confined to the patie nts (19.9 mu mol/L; 10.0-30.7, n = 9) with serum creatinine. levels > 100 m u mol/L, compared to those patients (9.6; 5.9-14.3 mu mol/L, n = 15) with a serum creatinine below 100 mu mol/L. None of the patients without or with minimal background retinopathy had serum creatinine levels > 100 mu mol/L. We conclude that diabetic retinopathy is not associated with increased plas ma homocysteine levels, but plasma homocysteine accumulates, probably owing to reduced glomerular filtration, in diabetic patients with signs of nephr opathy. In these patients, the promoting effect of nephropathy on the devel opment of retinopathy does not seem to be mediated through homocysteine.