Early neurovascular retinal changes detected by swept-source OCT in type 2 diabetes and association with diabetic kidney disease

• Autor(a) principal: Silva, Monica Oliveira da
• Data de Publicação: 2021
• Outros Autores: Chaves, Anne Elise Cruz do Carmo, Gobbato, Glauber Corrêa, Reis, Mateus Augusto dos, Lavinsky, Fábio, Schaan, Beatriz D'Agord, Lavinsky, Daniel
• Tipo de documento: Artigo
• Idioma: eng
• Título da fonte: Repositório Institucional da UFRGS
• Texto Completo: http://hdl.handle.net/10183/242309
• topic: Diabetes mellitus tipo 2; Taxa de filtração glomerular; Tomografia de coerência óptica; Retinopatia diabética; Diabetes mellitus type 2; Optical coherence tomography; Retinal neurodegeneration; Glomerular filtration rate; Diabetic retinopathy

Purpose To evaluate retinal thickness and capillary density in patients with type 2 diabetes (T2D) and their association with diabetic kidney disease (DKD) using swept-source optical coherence tomography (SS-OCT). Methods A cross-sectional study was conducted with T2D patients with mild or no diabetic retinopathy (DR) and nondiabetic controls. Inner retinal layer thickness was measured with SS-OCT. Retinal capillary density and the foveal avascular zone (FAZ) were measured with SS-OCT angiography (OCTA). SS-OCT parameters were compared in patients with and without diabetic kidney disease (DKD) and nondiabetic controls. Results 131 DKD eyes showed decreased ganglion cell layer plus (GCL+) (p = 0.005 TI; p = 0.022 I), retinal nerve fiber layer (RNFL) (p = 0.003), and central retinal thickness (CRT) (p = 0.032), as well as foveal avascular zone (FAZ) enlargement (p = 0.003) and lower capillary density in the superficial vascular plexus (p = 0.016, central quadrant), compared to controls. No statistically significant changes were found between diabetic patients without significant DKD and controls. Conclusion Our findings suggest early neurovascular damage in patients with T2D; these changes were more significant in patients with DKD. Larger longitudinal studies are warranted to determine the role of early neurovascular damage in the pathophysiology of severe DR.