Evaluation of Endothelial Dysfunction in Geriatric Patients with Non-Dialysis Chronic Kidney Disease

Background: Chronic kidney disease presents a significant health challenge among the elderly, with recent data indicating a 13.9% prevalence for early stages (1–3) and a lower 0.6% prevalence for advanced stages. Notably, many geriatric patients die from cardiovascular complications before reaching end-stage kidney disease, highlighting the critical interplay between renal and cardiovascular health. Central to this connection is endothelial dysfunction, considered the initial trigger for cardiovascular mortality. We aimed to investigate the correlation between different measurement methods demonstrating endothelial dysfunction and sVE-cadherin levels. Another objective was to examine the relationship between decreased glomerular filtration rate (GFR) and sVE-cadherin levels. We hypothesized an inverse relationship between impaired renal function, endothelial dysfunction, and sVE-cadherin. Methods: The study included geriatric patients with CKD who were not receiving RRT. Non-geriatric patients, those with cardiovascular disease, atrial fibrillation, heart failure, active immunosuppressive use, active infection, history of active malignancy, Raynaud’s phenomenon, and renal transplantation patients were excluded. Demographic data of the patients, nailfold capillary measurements, carotid intima-media thickness, flow-mediated dilatation, sVE-cadherin, and serum fibroblast growth factor 23 (FGF23) levels were measured. Results: We analyzed 96 patients. Key findings revealed a significant inverse correlation between serum sVE-cadherin levels and glomerular filtration rate (GFR), suggesting that, as kidney function declines, endothelial integrity is compromised. Interestingly, patients treated with sodium–glucose co-transporter-2 inhibitors had notably lower sVE-cadherin levels, indicating the possible modulatory effect of these drugs on endothelial function. Additional correlations were observed: fibroblast growth factor 23 levels were positively related to capillary diameter, and carotid intima-media thickness was associated with mean platelet volume. Declining GFR corresponded to reductions in capillary count, while use of dipeptidyl peptidase-4 inhibitors was linked to higher capillary density. Over a 2.3-year follow-up, survivors had higher lymphocyte counts (p = 0.088, not statistically significant) and baseline sVE-cadherin levels tended to be higher in those who died, although this was not statistically significant. Conclusions: These findings suggest that uremic toxins may worsen endothelial injury by disrupting intercellular connections, highlighting the complex pathogenic environment in CKD. Given these insights, the need for standardized diagnostic thresholds for endothelial dysfunction in geriatric CKD patients is clear. Serum sVE-cadherin emerges as a promising novel biomarker for assessing endothelial health, offering potential for earlier intervention and improved cardiovascular outcomes. It may be a potent indicator of endothelial dysfunction and should be featured in future studies of elderly CKD patients.