Our study revealed that Syndecan-1 levels significantly predict severe acute kidney injury and its prognosis following cardiac surgery. This research underscored the crucial role of endothelial damage in the pathogenesis of post-surgical AKI, demonstrating SDC-1’s superior predictive value over traditional inflammatory markers. These insights contributed to a broader understanding of AKI mechanisms and advocate for the integration of SDC-1 monitoring in postoperative care, enhancing early detection and intervention strategies and potentially improving patient outcomes in the cardiac surgery population.

Our analysis aligns with prior research on SDC-1’s predictive value for AKI but extends the understanding to adult cardiac surgery patients, highlighting its specificity and reliability beyond established literature. While previous research has established SDC-1 as a marker of endothelial injury and its potential in AKI prediction [6,7,8, 13, 14], our findings further delineate its specificity and reliability post-cardiac surgery. Previous studies on SDC-1 and AKI have primarily focused on pediatric cardiac surgery patients [7]. In contrast, our study encompasses adult cardiac surgery patients, covering not only coronary artery bypass but also valve surgeries, particularly those requiring cardiopulmonary bypass. Our methodology, encompassing a comprehensive analysis of SDC-1 levels alongside traditional inflammatory markers, provided a novel comparative perspective previously underexplored. The outcomes of our study, especially the superior predictive value of SDC-1 for progressive AKI and AKI-KRT, underscored the importance of endothelial damage in AKI pathogenesis, suggesting a unique injury pathway in cardiac surgery patients less prevalent in broader AKI research.

Elevated SDC-1 levels’ link to severe AKI underscores the pivotal role of endothelial damage in AKI’s pathogenesis, reflecting the early and critical events leading to renal complications post-surgery [14]. SDC-1, indicative of endothelial glycocalyx integrity, increases in response to endothelial injury, a critical early event in AKI pathogenesis. This damage facilitates inflammation, enhances vascular permeability, and disrupts renal microcirculation, contributing to kidney injury [15]. The cardiopulmonary bypass process, common in cardiac surgeries, contributes to systemic inflammation [16] and endothelial dysfunction [17, 18]. This may result in shedding of endothelial glycocalyx components, such as Syndecan-1, into the bloodstream, indicating vascular damage potentially leading to complications like AKI [15]. Furthermore, SDC-1 may interact with other molecular markers, including inflammatory cytokines and coagulation markers [19, 20], exacerbating endothelial dysfunction and AKI severity. Understanding these interactions is crucial to developing targeted therapies to mitigate AKI progression post-cardiac surgery.

By incorporating inflammatory cytokines, we enhanced the comprehensive understanding of inflammatory processes and endothelial injury mechanisms contributing to AKI post-cardiac surgery. This approach enhanced the predictive framework for AKI, offering deeper insights into patient-specific risk factors and potential therapeutic targets, thus broadening the scope of AKI management strategies in the clinical setting.

Our comparison between SDC-1 and cytokines elucidates different aspects of AKI risk, suggesting SDC-1’s superior predictive value could lead to more effective early interventions in post-surgical AKI. While SDC-1 directly reflected endothelial injury, cytokines indicate generalized inflammation. This comparison could delineate specific versus systemic responses to surgical stress, thus enhancing AKI prediction accuracy. The merit lied in the potential to identify a more reliable biomarker for early intervention, thereby improving patient outcomes by more effectively targeting the underlying mechanisms of AKI. SDC-1 may offer superior predictive value over traditional inflammatory markers due to its direct involvement in endothelial injury [21], a critical early event in AKI pathogenesis. Unlike inflammatory markers that indicates a general response to injury or infection, SDC-1 specifically reflects the endothelial glycocalyx condition, providing a more direct assessment of endothelial health and AKI potential. Studies comparing AKI biomarkers have highlighted endothelial damage’s role in AKI development, suggesting that markers like SDC-1, closely related to endothelial integrity, might provide earlier and more specific predictive capabilities for AKI after cardiac surgery [6,7,8,9, 13].

Our findings indicated that elevated SDC-1 levels are associated not only with the incidence and severity of AKI but also with prolonged ICU and hospital stays. This association underscored the broader impact of endothelial injury, as indicated by SDC-1 levels, on patient recovery and healthcare resource utilization, highlighting the need for early detection and intervention strategies to mitigate adverse outcomes associated with cardiac surgery-associated AKI.

The study evaluated 122 eligible patients. To ascertain the adequacy of this sample size, a power analysis was conducted prior to the study. Assuming an expected effect size derived from preliminary studies or literature, we aimed for an 80% power to detect significant differences with a two-sided alpha of 0.05. Based on these parameters, our power analysis indicated that a sample size of 122 patients is sufficient to detect the expected effect size regarding the primary outcome of severe AKI incidence post-cardiac surgery. This ensures that our study had the necessary statistical power to test our primary hypothesis effectively.

While our study provides valuable insights, its single-center nature and limited sample size call for further validation across different populations and clinical settings to ensure broader applicability. These limitations implied that our results may not fully represent the broader population undergoing cardiac surgery. Future research should concentrate on multi-center studies to validate our findings across diverse patient demographics and clinical practices. Longitudinal analyses of SDC-1 levels over time would provide insights into their dynamics relative to AKI progression. It is worth noting that our study did not include common AKI biomarkers because our aim was to ascertain the association between SDC-1 and severe AKI, thereby laying the groundwork for future exploration of the mechanisms of AKI onset and progression from the perspective of endothelial damage. Furthermore, investigating interventions for patients identified as high-risk based on SDC-1 levels could inform targeted strategies to mitigate severe AKI outcomes.