Reliability and validity of digital assessment of perifoveal capillary network measurement using high-resolution imaging.

BACKGROUND: Assessment of the perifoveal capillary network (PCN) might indicate macular function and could reflect the systemic microcirculation. The quantification and reliability of this measurement is currently unknown. The aim of this study was to validate quantification of the PCN by a non-invasive technique from high-resolution retinal images. METHODS: Ten healthy volunteers were included in this validation study. At least 320 high-resolution retinal images were used for assessment of inter- and intra-observer reliability. Non-invasive capillary perfusion mapping was performed using a retinal function imager. After the images were enhanced and segmented, the reproducibility was verified by comparing the values of two independent examiners and of a single examiner at two different time points. RESULTS: The inter-observer concordance coefficients were highly significant for PCN (intraclass correlation coefficient (ICC)=0.901, 95% CI 0.655 to 0.975, p<0.001) and normalised PCN (ICC=0.727, 95% CI 0.262 to 0.923, p=0.004). The intra-observer measurements at two different time points were also highly concordant for PCN (ICC=0.879, 95% CI 0.598 to 0.968, p<0.001) and for normalised PCN (ICC=0.960, 95% CI 0.851 to 0.990, p<0.001). CONCLUSIONS: The reliability of PCN measurement is reproducible and could be used as a new tool to quantify the capillary perfusion network of the macular area.

The contribution of hypertension to diabetic nephropathy and retinopathy: the role of inflammation and oxidative stress.

Diabetes and hypertension frequently coexist and constitute the most notorious combination for the pathogenesis of diabetic nephropathy and retinopathy. Large clinical trials have clearly demonstrated that tight control of glycemia and/or blood pressure significantly reduces the incidence and progression of diabetic retinopathy (DR) and nephropathy. However, the mechanism by which hypertension interacts with diabetes to induce and/or exacerbate nephropathy and retinopathy is very unclear. Substantial evidence implicates the involvement of chronic inflammation and oxidative stress in the pathogenesis of DR and nephropathy. In addition, hypertension causes oxidative stress and inflammation in the kidney and retina. In the present review, we summarized data obtained from our research along with those from other groups to better understand the role of hypertension in the pathogenesis of diabetic nephropathy and retinopathy. It is suggested that oxidative stress and inflammation may be common denominators of kidney and retinal damage in the concomitant presence of diabetes and hypertension.

A decrease in retinal progenitor cells is associated with early features of diabetic retinopathy in a model that combines diabetes and hypertension.

PURPOSE: Hyperglycemia and hypertension contribute to the development of diabetic retinopathy, and this may involve alterations in the normal retinal cell cycle. In this work, we examined the influence of diabetes and hypertension on retinal cell replication in vivo and the relationship between these changes and several early markers of diabetic retinopathy. METHODS: Diabetes was induced with streptozotocin in 4- and 12-week-old spontaneously hypertensive rats (SHR) and their Wistar Kyoto (WKY) controls. The rats were killed 15 days later. Retinal cells stained with bromodeoxyuridine (BrdU) were seen in rats of both ages. RESULTS: In 12-week-old rats, the number of BrdU-positive retinal cells was higher in SHR than in WKY rats. After 15 days of diabetes mellitus, there was a marked reduction in cell replication only in diabetic SHR (p=0.007). The BrdU-positive cells expressed neural, glial, or vascular progenitor markers. There was greater expression of p27(Kip1) in the ganglion cell layer of both diabetic groups (p=0.05), whereas in the inner nuclear layer there was enhanced expression only in diabetic SHR (p=0.02). There was a marked increase in the retinal expression of fibronectin (p=0.04) and vascular endothelial growth factor (p=0.02) in diabetic SHR that was accompanied by blood-retinal barrier breakdown (p=0.01). DISCUSSION: Concomitant diabetes and hypertension attenuated the proliferation of retinal cells, and it is associated with an increase in p27(Kip1) expression, fibronectin accumulation, and blood-retinal barrier breakdown. The replicative retinal cells displayed characteristics of progenitor cells.