With rising percutaneous coronary intervention (PCI) volumes, particularly among elderly patients, PCI is increasingly extended to more complex vessel diseases. The number of severely calcified coronary lesions during PCI has increased significantly. Severely calcified coronary lesions are a significant clinical challenge for PCI. Stent implantation failure and incomplete expansion—common consequences of severe coronary calcium—significantly diminish PCI success rates longitudinally. Rotational atherectomy (RA) constitutes a cornerstone strategy for managing these complex lesions [1, 2]. The use of RA to pretreat severely calcified coronary lesions can improve the efficiency of interventional surgery, reduce complications of interventional procedures, increase the success rate of PCI [3], and may also reduce long-term in-stent restenosis.

Contrast-induced nephropathy (CIN) is characterized by an abrupt decline in kidney function precipitated by intra-arterial or intravenous contrast injection [4]. It is currently the third leading cause of acute renal deterioration in hospitals, following reduced renal perfusion and acute renal failure [1]. While interventional procedures pose minimal renal risk in the general population, substantially elevated nephrotoxicity hazards exist in vulnerable subgroups, notably among cardiac surgery patients. Reported rates can vary considerably between centers [2, 3, 4, 5, 6]. CIN post-PCI is related to increased risk of mortality and dialysis, as well as recurrent myocardial infarction and target vessel reconstruction [6]. Given the current absence of proven therapies for CIN combined with the scarcity of preventive strategies validated by randomized controlled trials, developing effective renal protective protocols remains a critical unmet need in interventional medicine [2]. Therefore, risk stratification, prevention, and treatment of CIN are of clinical importance, and CIN remains a hot topic of concern to clinicians.

Established predictors of contrast-induced nephropathy encompass pre-existing renal dysfunction, diabetic comorbidity, advanced age, and impaired cardiac function [7], among which hemodynamic instability is also an important risk factor. In particular, perioperative hypotension and the use of intra-aortic balloon pumps could increase the risk of CIN, which may be related to low mean arterial pressure (MAP) leading to insufficient renal perfusion [8, 9]. Abnormal blood pressure (including hypertension and hypotension) may affect the risk of CIN through multiple mechanisms. On the one hand, long-term hypertension can lead to renal vascular sclerosis, microcirculatory disorders, and endothelial dysfunction, weakening the kidney’s ability to compensate for ischemia and toxins. Epidemiological data show that the incidence of CIN in hypertensive patients is 1.5–2 times higher than that in normal blood pressure patients, and poor blood pressure control (such as systolic blood pressure $>$160 mmHg) is associated with more severe renal damage. On the other hand, perioperative hypotension (such as systolic blood pressure 90 mmHg) may cause insufficient renal perfusion and aggravate medullary hypoxia and oxidative stress caused by contrast media. This “double-edged sword” effect makes blood pressure monitoring and management a key issue for the prevention of CIN: it is necessary to avoid vascular damage related to hypertension, and to maintain adequate perfusion pressure to protect renal function [10]. Patients undergoing PCI for moderately or severely calcified lesions have an increased prevalence of renal insufficiency [11]. Caution in the usage of contrast media is appropriate in these cases to reduce the risk of CIN. Compared with ordinary PCI patients, patients undergoing RA often have multiple comorbidities, longer procedure time, and higher contrast media dose. At present, there are no relevant clinical reports on the impact of blood pressure on CIN after PCI in patients undergoing RA. This study retrospectively analyzed the risk factors for CIN in patients with coronary heart disease who underwent RA, focusing on the blood pressure indicators, providing related information that adds to the early screening, identification, and management decision-making of CIN in patients undergoing RA.

Limited data exist on risk factors for CIN following RA. Our findings revealed that a history of diabetes, a history of hypertension, preoperative GFR, the presence or absence of heart failure, intraoperative use of IABP, and contrast volume were not risk factors for CIN in patients undergoing RA procedures. However, a preoperative MAP 80 mmHg was significantly associated with an increased risk of postoperative CIN. After adjusting for confounders, the incidence of MACCE and secondary endpoints in the CIN group was comparable to that in the non-CIN group. Consequently, patients with preoperative MAP 80 mmHg undergoing RA require intensified vigilance—including proactive screening and early intervention for CIN—to mitigate associated risks.

CIN and cholesterol crystal embolism (CCE) can both manifest as renal insufficiency following vascular interventional procedures, yet they differ fundamentally in nature. CIN is essentially an acute toxic injury to the renal tubules, induced by the direct cytotoxicity of iodinated contrast agents and ischemia in the renal medulla. It has a short latency period (24–72 hours), presenting as a transient elevation in serum creatinine (Scr) that typically resolves within 7–10 days in most patients. Urinary sediment may show renal tubular epithelial cells. It lacks extrarenal manifestations. The primary risk factors are pre-existing renal insufficiency and diabetes. CCE, conversely, is fundamentally an embolic vascular injury. It originates from the rupture of atherosclerotic plaques, leading to cholesterol crystals obstructing the renal arterioles. CCE usually becomes clinically evident after a relatively long latency period, typically presenting with a progressive and often irreversible increase in Scr within 1 to 4 weeks after contrast administration [15]. In this study, all 16 patients with CIN exhibited elevated Scr within 24 to 72 hours after surgery. One of these patients, who required permanent dialysis, already had stage 3b renal function before the procedure. None of the CIN patients developed peripheral eosinophilia or showed systemic embolic manifestations involving multiple organs, such as livedo reticularis (a net-like bluish-purple rash), digital gangrene, intestinal ischemia, or retinal Hollenhorst plaques—systemic features that may occur in CCE. Definitive exclusion of CCE may ultimately rely on biopsy (of skin, muscle, or kidney), where “needle-shaped clefts” left behind after the dissolution of cholesterol crystals can be observed within small arteries.

Literature shows that one-fifth of patients undergoing PCI have moderate or severe coronary artery calcification [11]. Using RA to treat severely calcified coronary lesions can make the stent obtain a larger diameter, a larger lumen cross-sectional area, and less final residual stenosis [10]. Patients undergoing RA also have a higher procedural success rate [3, 11]. Given these advantages, a growing number of interventional cardiologists now utilize RA for severely calcified coronary lesions. However, RA is related to higher technique demand, prolonged procedural time, higher radiation dose, and contrast media dose [3]. Clinical data are lacking regarding whether longer operation time and higher contrast media dose causally affect the incidence of CIN, the incidence, and related risk factors of CIN in patients undergoing RA. Our results showed that among 111 coronary heart disease patients who underwent RA, 16 developed CIN, representing an incidence rate of 14.41%. Notably, a previous study reported a CIN incidence rate of 19.51% [16] in coronary heart disease patients after PCI. Although the CIN incidence observed in this study is numerically similar to or a little bit lower compared to historical data, indicating similar incidence with or without RA, directly comparing the incidence of CIN is not possible because the characteristics of patients in this and previous studies might be different. The data should thus be interpreted with great caution due to potential significant differences in patient baseline characteristics.

MAP is an important physiological index reflecting organ perfusion, and it has a complex relationship with the occurrence and development of CIN. The pathological mechanism of CIN involves renal hemodynamic disturbances, tubular toxicity damage, and oxidative stress [12, 13, 17, 18], the risk of CIN through multiple pathways. A critically low MAP may significantly reduce renal blood flow, compromising the kidney’s autoregulatory capacity—particularly the balance of oxygen supply and demand in the renal medulla [10]. Studies indicate that contrast media can cause transient early vasodilation followed by sustained vasoconstriction, further diminishing medullary blood flow [19, 20]. Under low MAP conditions, this process exacerbates medullary hypoxia and increases the risk of acute kidney injury [21]. Our study also confirmed that the incidence of CIN in patients with concomitant heart failure (84.6%) was significantly higher than that in the non-heart failure group (38.5%). Early studies indicate that hemodynamic alterations secondary to cardiac dysfunction—specifically reduced cardiac output and intravascular volume—represent a key underlying mechanism of CIN [22, 23]. The hemodynamic alterations stemming from cardiac dysfunction—primarily characterized by diminished cardiac output and reduced intravascular volume—establish a direct pathophysiological link to decreased MAP. According to the fundamental equation MAP = Cardiac Output (CO) $\times$ Systemic Vascular Resistance (SVR), reductions in CO directly lower MAP. And MAP values 80 mmHg in such patients correlate with heightened risks of renal hypoperfusion and contrast-induced nephropathy.

Optimized hemodynamic management serves not only renal protection but also as a core cardiorenal preservation strategy. Given the critical importance of maintaining optimal MAP, continuous hemodynamic monitoring and targeted titration of MAP are clinically imperative, as both hypotension and hypertension can compromise renal function through distinct mechanisms. Comprehensive risk mitigation thus necessitates holistic evaluation of comorbidities, hemodynamic profiles, and contrast exposure parameters, integrating MAP optimization, adequate hydration, and personalized pharmacotherapy. To operationalize this paradigm, patients undergoing RA procedures require preoperative risk stratification, perioperative titration of MAP, and postoperative renal function monitoring. Furthermore, large-scale multi-center studies are needed to establish population-specific MAP targets and evidence-based intervention thresholds [24]. Ultimately, modulation of this modifiable risk factor promises significant reductions in CIN and associated cardiorenal adverse events.

Shortcomings and prospects of the present study: (1) The single-center design and limited cohort constrain the generalizability of these observations. External validation through multi-center collaborations is imperative. (2) At present, the pathological and physiological mechanisms of CIN after PCI have not been fully elucidated, and further research is still needed in subsequent studies.

Once CIN is established, only supportive care is currently provided until renal function resolves. Therefore, presently, the main method to tackle this complication is its prevention. Preprocedural MAP 80 mmHg constitutes an independent risk factor for CIN following coronary RA, establishing a pivotal therapeutic target for precision perioperative management. This evidence mandates the integration of preoperative blood pressure assessment into standardized RA patient risk stratification protocols. Early identification of high-risk cohorts (MAP 80 mmHg) enables proactive intervention during the preprocedural window through individualized volume expansion and judicious vasoactive agent administration to elevate MAP to the safety threshold ($\ge$80 mmHg), thereby intercepting CIN pathogenesis at its origin. Therefore, for patients undergoing coronary RA with preoperative MAP 80 mmHg, intensified perioperative MAP monitoring and early implementation of preventive measures against CIN are essential to mitigate the risk of adverse clinical events.

The datasets used and analyzed during the current study are available from the corresponding author on reasonable request.

XGL, LW, XYW, and YG: study design, data collection, data analysis, writing original draft. XGL and YG: Obtained funding. XGL and LQH: methodology, supervision, funding acquisition, writing—review & editing. All authors contributed to editorial changes in the manuscript. All authors read and approved the final manuscript. All authors have participated sufficiently in the work and agreed to be accountable for all aspects of the work.

Ethics approval was obtained from the Ethics Committee of Wuhan Fourth Hospital, the ethics certificate number is KY2024-124-01, and all of the participants provided signed informed consent. The study was conducted in accordance with the amended Declaration of Helsinki.

This study was funded by Hubei Provincial Natural Science Foundation of China (2022CFB512).

The authors declare no conflict of interest.