In this study, we investigated the predictive value of perioperative serum albumin levels for the occurrence of CI-AKI in CHD patients after PCI. We found that the incidence of CI-AKI in the high &Alb group was significantly greater than that in the low &Alb group. The AUC of &Alb for detecting CI-AKI after PCI was 0.675 (95% CI = 0.627–0.724, P < 0.001), with a sensitivity of 70.7%. We demonstrated that decreased perioperative albumin levels (&Alb ≥ 4.55 g · L− 1) were an independent risk factor for CI-AKI and an important predictor of MACEs 1 year after PCI in patients with CHD; &Alb ≥ 4.55 g · L− 1 could not only be used for the early identification of CI-AKI in the short term after PCI in patients but also had high predictive value for MACEs 1 year after PCI.

Contrast agents are commonly used to enhance imaging, particularly in computed tomography and magnetic resonance imaging, as well as in coronary angiography (CAG) and percutaneous coronary intervention (PCI) [12, 23]. In patients undergoing PCI, CI-AKI has emerged as a serious complication closely related to clinical adverse events, increasing morbidity and mortality rates [3, 5, 24]. The clinical and surgical prognosis of patients with CHD is significantly improved by the use of coronary stenting [25]. However, the incidence of CI-AKI is increasing annually, and CI-AKI has become a critical complication of coronary revascularization. Our results showed that CI-AKI increases the occurrence of MACE and significantly affects the clinical prognosis of patients after PCI. The pathogenesis of CI-AKI is complex, and the specific pathophysiologic basis remains unclear. At present, this effect is primarily attributed to intrarenal vasoconstriction, the production of reactive oxygen species, and direct tubular injury. After intravascular injection of contrast media, various factors can lead to renal vasoconstriction, including antidiuretic hormone (ADH), adenosine, and endothelin-1 (ET-1) [26]. These factors transiently increase renal arterial blood flow, followed by persistent severe contraction, eventually causing renal hypoperfusion, renal medullary ischaemia, and hypoxia [27]. Oxidative stress injury may also be one of the pathophysiological mechanisms of CI-AKI. The contrast agent can lead to a reduction in blood supply to the renal medulla, causing an imbalance between metabolic demand and blood supply in the thick ascending limb of the Henle loop in the outer medullary layer. This imbalance results in the generation of superoxide, leading to oxidative necrosis of the renal tubules [28, 29]. Direct cytotoxicity of contrast agents in vascular endothelial cells leads to elevated levels of endothelin and adenosine, reduced nitric oxide and prostaglandins [30], and increased fluid viscosity in vascular and tubular cells. Although the majority of contrast media-induced kidney damage can return to normal levels within 1 to 4 weeks, several risk factors, such as CKD and hypotension, may result in the loss of functional nephrons and impairment of renal function. As the dose of contrast medium increases, the regenerative capacity of tubular epithelial cells is compromised, leading to potential fibrosis and permanent loss of function in some renal units [31, 32]. Contrast agents act as allergens, triggering systemic allergic reactions and renal immune inflammatory responses and playing a role in the mechanisms of CI-AKI [28]. Systemic inflammation can render the kidney more vulnerable to local inflammation induced by iodinated contrast agents after angiography, thereby exacerbating the development of contrast-induced acute kidney injury.

Vascular remodelling induced by oxidative stress and the secondary inflammatory response is the central link in the chain of events in CHD. Endothelial dysfunction and an imbalance in smooth muscle phenotype conversion are two key factors in vascular remodelling. Atherosclerosis is associated with several susceptibility factors for CI-AKI and results in the release of reactive metabolites that can induce haemodynamic and inflammatory changes, further compromising renal blood flow. As one of the routine examinations for hospitalized patients, serum albumin plays a crucial role in binding and transporting endogenous and exogenous substances in the body. It helps maintain stable colloid osmotic pressure in the blood, eliminates free radicals harmful to the body, and inhibits platelet aggregation to achieve an anticoagulant effect [33]. Low levels of serum albumin can lead to the cytotoxicity and strong atherogenic effects of oxidatively deformed LDL [34]. Conversely, reduced albumin expression can increase blood viscosity, thereby promoting the progression of CHD and disrupting normal vascular endothelial function, ultimately impairing cardiac function. As indicators of nutritional status and inflammatory factors, perioperative albumin levels and postoperative outcomes were investigated. Several previous studies have shown that perioperative albumin levels are significantly associated with postoperative complications in patients with malignancies, such as colorectal cancer, gastric cancer, and lung cancer, as well as in noncancer patients [13, 15, 17, 18]. Similarly, the relationship between perioperative albumin levels and adverse outcomes after abdominal surgery has been discussed [17, 18].

The incidence of CI-AKI in patients after PCI was found to be as high as 15.3% in this study, making early identification of patients at risk for CI-AKI extremely important. In terms of CI-AKI, our findings are largely consistent with the results from a clinical study in which 890 ACS patients were enrolled and underwent primary PCI, indicating that lower serum albumin levels may predict CI-AKI development after primary PCI in ACS patients [8]. Moreover, multivariate logistic regression analysis revealed that a high &Alb level (OR 2.495, 95% CI: 1.277–4.874, P = 0.007) can predict CI-AKI development after primary PCI in CHD patients. Receiver operating characteristic curve analysis revealed that the &Alb level is an accurate predictor for the development of CI-AKI. The area under the curve was 0.675 for the baseline &Alb level (95% CI: 0.627–0.724, P < 0.001). The optimal cut-off point of &Alb was 4.55 g/L, with a sensitivity of 70.7% and a specificity of 58.5%. These findings suggest that a reduction in perioperative serum albumin levels can serve as a predictor of CI-AKI following PCI. This can aid in the early identification of patients undergoing PCI who are at high risk of developing CI-AKI, laying the groundwork for implementing preventive strategies. For patients with decreased serum albumin levels during the perioperative period, it is necessary to maintain sufficient mean arterial pressure, supplement albumin, and administer medication to reduce extravascular protein leakage. More samples and studies are needed to further prove this point.

By comparing the baseline data of the two groups of patients, we also found that the patients in the high &Alb group were older and had lower body mass index values. This observation suggests that the postoperative reduction in albumin levels was more pronounced in older patients than in younger patients, which may be associated with low food intake and poor nutritional status in elderly patients. Serum albumin levels are primarily used to assess malnutrition and chronic diseases. A low level of serum albumin can result in decreased plasma colloid osmotic pressure, excessive fluid accumulation in the interstitial space, reduced effective circulating blood volume, microcirculatory disturbances, hypoperfusion of vital organs, and potentially multiple organ dysfunction. This suggests that we should direct more attention to the nutritional status of elderly patients before surgery.

At the 1-year follow-up, the incidence of MACEs was greater in the high &Alb group than in the low &Alb group. Cox regression analysis revealed that CI-AKI was an independent predictor of the primary endpoint outcome, indicating that CI-AKI is associated with an increase in MACEs in CHD patients. CI-AKI is strongly linked to a poor prognosis. The results of this study highlight the importance of CI-AKI in the incidence of MACEs.

This study has several limitations. First, all patients in the current study came from one hospital, so the sample size was small, and selection bias was inevitable. This issue needs to be addressed by collecting data from a larger sample size to further demonstrate its impact. Furthermore, many factors can affect albumin levels and/or the incidence of myocardial infarction. Although many disease states that may affect the final results were excluded from this study and multifactor adjustments were performed to reduce bias, there may still be other confounding factors that were not adjusted for during enrolment, which may have affected the results.