Acute kidney injury (AKI) remains one of the most serious complications following cardiac surgery, particularly coronary artery bypass grafting (CABG). This comprehensive scoping review examines the role of central venous pressure (CVP) as a contributing hemodynamic factor in the development of cardiac surgery-associated AKI (CSA-AKI). Drawing from 16 studies published between 2016 and 2024, the review provides a detailed synthesis of current evidence while identifying gaps that warrant further investigation.
The incidence of AKI after cardiac surgery ranges widely from 10% to 40%, significantly increasing patient mortality, length of hospital stay, and healthcare costs. Traditionally, the focus has been on maintaining adequate arterial perfusion, particularly mean arterial pressure (MAP), to prevent renal injury. However, emerging evidence suggests that venous congestion—reflected by elevated CVP—plays an equally critical and underrecognized role in renal dysfunction.
This review followed PRISMA-ScR guidelines and the Arksey and O’Malley framework, ensuring methodological rigor. A total of 1,717 studies were initially identified, with 16 meeting strict inclusion criteria after screening. As illustrated in the flow diagram on page 5, the selection process emphasized studies that included standardized AKI definitions and quantitative CVP measurements.
The findings consistently demonstrate that elevated CVP is associated with an increased risk of postoperative AKI. Reported CVP thresholds varied, with intraoperative values ranging from 6.5 to 12 mm Hg and postoperative values from approximately 6.6 to 10.3 mm Hg. Despite this variability, a clear trend emerged: higher CVP levels correlate with worse renal outcomes. The strongest associations were observed in postoperative measurements, suggesting that sustained venous congestion after surgery may be particularly harmful.
Mechanistically, elevated CVP contributes to AKI through several pathways. Increased venous pressure reduces the renal arteriovenous pressure gradient, impairing blood flow and glomerular filtration. Additionally, intrarenal congestion increases interstitial pressure, further compromising kidney function. The review also highlights inflammatory mechanisms, including neutrophil accumulation and activation of neurohormonal systems such as the renin–angiotensin–aldosterone axis.
A particularly important finding is the synergistic relationship between elevated CVP and low MAP. Several studies demonstrated that patients experiencing both conditions had a significantly higher risk of AKI compared to those with isolated abnormalities. This underscores the importance of a balanced hemodynamic approach, rather than focusing solely on arterial pressure.
The table on page 6 provides a comprehensive overview of included studies, detailing sample sizes, CVP measurement timing, and AKI criteria. Most studies utilized KDIGO definitions, although some used RIFLE or other criteria, contributing to heterogeneity. This variability, along with differences in study design (predominantly retrospective cohorts), limits the ability to establish causality or define universal CVP thresholds.
Despite these limitations, the review highlights important clinical implications. CVP monitoring, already widely used in cardiac surgery, may serve as a valuable tool for identifying patients at risk of AKI. However, the authors caution against using CVP in isolation. Instead, it should be integrated with other hemodynamic parameters such as MAP, cardiac output, and fluid balance to guide individualized patient management.
The study also identifies key areas for future research. Standardization of CVP measurement protocols is essential to improve comparability across studies. Additionally, prospective multicenter trials are needed to validate CVP thresholds and assess whether CVP-guided interventions—such as fluid restriction or diuretic therapy—can reduce AKI incidence.
In conclusion, this scoping review provides compelling evidence that elevated CVP is associated with increased risk of AKI following cardiac surgery. While the findings support the potential role of CVP as a perioperative marker, significant heterogeneity and reliance on observational data limit definitive clinical recommendations. Future research should aim to refine CVP-based risk stratification and develop targeted interventions to improve renal outcomes in this high-risk population. Â
