RAAS Activation Linked to Vascular Stiffening in T1D With Proliferative Retinopathy

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The relationships between eye, nerve, and renal complications and the influence of RAAS activation after prolonged duration of T1D have not been well studied.
The relationships between eye, nerve, and renal complications and the influence of RAAS activation after prolonged duration of T1D have not been well studied.

In patients with long-standing type 1 diabetes (T1D) and proliferative diabetic retinopathy, renin-angiotensin-aldosterone system (RAAS) activation may be associated with vascular stiffening, according to study findings published in Diabetes Care.

While several studies have examined diabetic retinopathy in T1D, the relationships between eye, nerve, and renal complications and the influence of RAAS activation after prolonged duration of the disease have not been well examined. In this study, researchers assessed the relationship between retinopathy stage and other vascular complications before and after physiologic RAAS activation in adults with long-term (≥50 years) T1D. The 75 study participants underwent retinal examination by digital fundoscopic photography and were classified as having nonproliferative diabetic retinopathy, proliferative diabetic retinopathy, or no diabetic retinopathy. The presence of diabetic macular edema was determined via optical coherence tomography.

Of the participants, 12 (16%) had no diabetic retinopathy, 24 (32%) had nonproliferative diabetic retinopathy, and 39 (52%) had proliferative diabetic retinopathy. A low overall prevalence (4%) of diabetic macular edema was observed. Patients with proliferative diabetic retinopathy had worse nerve function and reduced corneal nerve density and were more likely to have macrovascular disease. After RAAS activation with high-dose angiotensin II, patients with proliferative diabetic retinopathy had increased arterial stiffness vs patients with nonproliferative diabetic retinopathy or no diabetic retinopathy. Following stimulation with low-dose angiotensin II, renal hemodynamic function and systemic hemodynamics remained comparable across the groups.

“Although it is not possible to determine why some patients in this cohort developed [proliferative diabetic retinopathy] while others did not after similar durations of type 1 diabetes, it seems unlikely that glycemic control alone is sufficient to fully explain the observed between-group differences and differing vascular risk profiles,” wrote the researchers.

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Reference

Lovshin JA, Lytvyn Y, Lovblom LE, et al. Retinopathy and RAAS activation: results from the Canadian Study of Longevity in Type 1 Diabetes. Diabetes Care. 2018;dc181809.

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