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Diabetic retinopathy and nephropathy share pathophysiological mechanisms and there is a defined correlation between the severity of both these microvascular complications from suboptimal glycaemic control. The reno-protective properties offered by sodium–glucose co-transporter-2 inhibitors and glucagon-like peptide-1 receptor agonists should be applicable to diabetic retinopathy as well. However, in patients with pre-existing diabetic retinopathy, sudden improvement in glycaemic control is well documented to cause early worsening of the changes in the retina that is usually transient. This paradoxical phenomenon tends to occur with longer duration of diabetes, higher HbA1c at the outset, rapid improvement of glucose levels and the magnitude of HbA1c reduction with addition of more agents to tighten metabolic control. Interestingly, this progression of pre-existing diabetic retinopathy is not quite observed with newer sodium–glucose co-transporter-2 inhibitors. This article discusses potential further areas of future research where mechanisms of renal protection can be translated to the retina.
Jacob et al. (Fri,) studied this question.