In our study, we examined the relationship between thickness of the chorioretinal layers measured using SD-OCT and the stages CKD in 72 patients with 144 eyes. We found that thinner retina and choroid were associated with CKD stage 3 and even more thinning in CKD stage 4–5. There was no association found between retinal and choroidal thickness and hypertension. However, we did observe associations between CRP and albuminuria, which were inversely correlated with choroidal thickness in CKD and were independent predictors of thickness. These findings may be explained by the role of inflammation in the development of both vascular and renal disease.

In this study, it was found that the choroidal thinning is more pronounced in advanced CKD. This thinning may be a reflection of a direct microvascular insult. As the vessels of the choroid supply the outer retinal layers and the RPE, it is possible that retinal abnormalities may occur as a result of choroidal pathology. The choroid plays a vital role in retinal function, as it nourishes the outer half of the retina. Abnormal choroidal circulation can lead to retinal photoreceptor dysfunction and death. Many diseases such as central serous retinopathy (CSR), age-related macular degeneration (AMD), pathological myopia and Vogt-Koyanagi-Harada (VKH) disease are related to choroidal changes. Identifying choroidal changes accurately will enable proper assessment of many posterior segment diseases. However, unlike the retina, choroidal structures do not have distinct, ordered layers and lack contrasting reflective properties, making it difficult to examine the choroid in as much detail as the retina [6]. Additionally, it is suggested that the disturbance of the autonomic nervous system may contribute to the changes observed. CKD is associated with increased sympathetic activity, which may play a role in the progression of the disease. While the choroidal circulation has autonomic innervation, the retinal circulation does not, thus the thinning of the outer retina and choroid might be related to increased sympathetic tone affecting the choroidal vasculature [7]. However, the study did not investigate the measurement of sympathetic activity.

Maria Vadalà and colleagues [7] conducted a study using swept source optical coherence tomography (SS-OCT) and optical coherence tomography angiography (OCTA) scans of the macular region to examine the association between retinochoroidal parameters and renal impairment in hypertensive, non-diabetic patients. They found that CKD is associated with thinning of both the retina and choroid, decrease in vascular density in both the superficial and deep perifoveal network, an inverse relationship between albuminuria and thickness of both the choroid and retina, and no correlation between blood pressure measurements and chorioretinal thicknesses and vascular density assessed by OCTA. Similarly, Ling Yeung and colleagues [8] assessed early retinal microvascular changes in patients with CKD via OCTA and reported significant retinal microvascular abnormalities such as blunt ended vessels, increased vascular tortuosity, and localized non-perfusion areas in patients with CKD.

In end stage renal disease, Ali Kal and colleagues [9] found that hemodialysis leads to a significant decrease in choroidal thickness, while there is no change in retinal thickness. This might be due to the extensive fluid absorption, which could affect ocular blood flow. A cross-sectional study conducted by Boem Changand et al. [10] also found a significant reduction in choroidal thickness at the macula and outside the macula, and this decrease in choroidal thickness was correlated with body weight loss, similar to the findings of Yang et al. [11]. The goal of hemodialysis is to maintain the kidneys’ excretory functions in ESRD patients, but during a hemodialysis session, ultrafiltration removes excess fluid from plasma, which leads to depletion of blood volume and an increase in the plasma protein concentration (rise of plasma colloid osmotic pressure), and a decrease in serum osmolality. This volume depletion is compensated by vascular refilling from the interstitial and intracellular space. As the choroid has a rich vascular network and the highest blood supply in the eye, these changes might affect its architecture [12]. In contrary to our study, Paterson and colleagues [1] reported that no significant associations were detected between choroidal volume or choroidal vascular index (CVI) and CKD, while the decrease in retinal thickness, particularly a thinner inner retinal layer, was found to be associated with CKD stage 4–5. Wu and colleagues [13] investigated retinal, neural and microvascular changes in different stages of CKD (stage 3–5) by SD-OCT and OCTA, and reported that retinal neural impairment was associated with decreased eGFR and more advanced CKD stage.

In our study, we found that there was no difference in Retinal nerve fiber layer (RNFL) thickness between the groups studied. This is in agreement with the findings of Craig Balmforth and colleagues [4], who conducted a study involving 150 subjects, including 50 patients with hypertension, 50 with CKD, and 50 matched healthy controls. They reported that retinal thickness, macular volume, and choroidal thickness were all reduced in CKD compared with hypertensive and healthy subjects. They also found that thinner choroid was associated with a lower estimated glomerular filtration rate (eGFR) and, in CKD, with proteinuria as well as increased circulating C-reactive protein, interleukin 6 (IL-6), asymmetric dimethylarginine (ADMA), and endothelin-1 (ET-1). However, Demir and colleagues [14] documented significant RNFL thinning in CKD without DM. Jung and colleagues [15] also reported reduction of thickness in the temporal and superior sectors of RNFL scan in patients with ESRD.

There were several limitations in this study. First, the medications taken by our patients, such as angiotensin-converting enzyme inhibitors, β-blockers, and statins may have had effects on the OCT parameters studied. However, all patients were stabilized on their therapies and this was an unavoidable limitation of such studies. Secondly, the lack of any angiographic examination which can study in deep the retinal and choroidal vascular structure like indocyanine green (ICG), fluorescein fundus angiography (FFA) and optical coherence tomography angiography (OCTA) which can study in deep the retinal and choroidal vascular structure. Also, the cross-sectional nature of this study does not allow for the determination of causality of association. Saying that, the clinical relevance of these findings requires further consideration through longitudinal evaluation of changes in retinal thickness with declining kidney function with age. Lastly, the specificity of the observed associations with the underlying cause of CKD was not examined. Longitudinal studies are needed to establish the chronological correlation with CKD severity. As well, focused studies on CKD subgroups based on the underlying pathology.