Acute kidney injury (AKI) is characterised by an abrupt decline in renal function, resulting in a reduction in glomerular filtration rate (GFR) and impaired clearance of metabolic waste products [1]. Beyond its immediate clinical consequences, AKI is associated with substantial medical, social, and economic burden for patients and healthcare systems [2]. Several patient-related factors, including advanced age, hypertension, hyperlipidemia, and peripheral vascular disease, may increase susceptibility to AKI. Cardiac surgery carries additional procedure-related risks owing to the use of cardiopulmonary bypass (CPB), prolonged cross-clamp (XC) time, exposure to blood products, and administration of high doses of vasopressors, all of which may contribute to renal hypoperfusion and kidney injury [1, 3]. AKI is therefore one of the most frequent complications following cardiac surgery and is associated with both short- and long-term adverse outcomes, including increased morbidity and mortality, even among patients who do not progress to renal failure [4, 5]. The reported incidence of AKI following cardiac surgery may be as high as 30%, while approximately 3% of patients may require dialysis or renal replacement therapy [3]. Previous studies have identified several potential predictors of postoperative AKI, including elevated preoperative serum creatinine (SCr) and prolonged duration of CPB [6]. Accurate identification and classification of AKI are essential for early recognition and risk stratification. The Risk, Injury, Failure, Loss of kidney function, and End-stage renal disease (RIFLE) classification assesses the severity of AKI based primarily on changes in SCr from baseline and has demonstrated an association with short-term mortality following cardiac surgery. Subsequent modifications incorporating the need for renal replacement therapy (RRT) into the failure stage have improved the predictive performance of the classification in patients undergoing cardiac surgery. In particular, the failure stage, defined by an increase in SCr to three times the baseline value or a reduction in GFR of more than 75%, has demonstrated superior predictive accuracy compared with the Acute Kidney Injury Network (AKIN) criteria when SCr is not corrected for fluid balance, which may otherwise result in overdiagnosis of AKI [4]. Contemporary definitions established by the Acute Dialysis Quality Initiative (ADQI), AKIN, and Kidney Disease: Improving Global Outcomes (KDIGO) emphasise the diagnosis of AKI using changes in SCr and urine output as key indicators of renal dysfunction [3]. Despite advances in perioperative management, postoperative AKI remains an important and potentially preventable complication of cardiac surgery. Identification of patient- and procedure-related risk factors may facilitate early recognition of high-risk individuals and support timely preventive and therapeutic strategies. Therefore, the present study was undertaken to assess the incidence, associated risk factors, and clinical outcomes of postoperative AKI among patients undergoing cardiac surgery at a single centre.

Study Design and Setting This retrospective observational study was conducted in the Department of Cardiothoracic and Vascular Surgery (CTVS), Indira Gandhi Institute of Medical Sciences (IGIMS), Patna, Bihar, India. The study included consecutive adult patients who underwent elective cardiac surgery during the predefined study period. Relevant clinical, laboratory, operative, and postoperative data were retrieved retrospectively from hospital medical records and electronic databases. The study was conducted in accordance with the ethical principles of the Declaration of Helsinki. Study Population The study population comprised consecutive adult patients undergoing elective cardiac surgery in the Department of Cardiothoracic and Vascular Surgery (CTVS), Indira Gandhi Institute of Medical Sciences (IGIMS), Patna, Bihar, during the period of two years i.e. July 2024 to June 2026. Patients were identified from the institutional surgical records and assessed for eligibility according to predefined inclusion and exclusion criteria. Only patients with adequate preoperative and postoperative clinical and laboratory records required for assessment of renal function were included in the final analysis. Inclusion criteria were: • Patients aged ≥18 years. • Patients undergoing elective cardiac surgery, including coronary artery bypass grafting (CABG) or valve replacement/repair surgery. • Availability of a documented preoperative baseline serum creatinine (SCr) value and adequate postoperative renal function data for assessment of AKI according to KDIGO criteria. Exclusion criteria were: • Patients aged <18 years. • Patients undergoing emergency cardiac surgery. • Patients receiving dialysis or renal replacement therapy before surgery. • Patients with incomplete or inadequate preoperative or postoperative renal function data that precluded reliable assessment of postoperative AKI. Patients fulfilling the eligibility criteria were included in the study and subsequently categorized into AKI and non-AKI groups based on the occurrence of postoperative AKI according to the KDIGO criteria. This approach enabled comparison of baseline characteristics, perioperative variables, and clinical outcomes between patients who developed postoperative AKI and those who did not. Sample Size Calculation As this was a retrospective observational study, all consecutive eligible adult patients undergoing elective cardiac surgery during the predefined two-year study period were considered for inclusion. Based on the previously reported incidence of postoperative acute kidney injury of approximately 27.5% by Mohrag et al. [7], a similar event rate was anticipated in the present cohort. A total of 100 patients fulfilling the predefined inclusion and exclusion criteria and having complete perioperative and renal function data were available and were included in the final analysis. With an expected AKI incidence of approximately 27.5%, this sample was anticipated to yield about 27–28 AKI events, allowing estimation of the incidence and exploratory assessment of associated perioperative risk factors. Data Collection Data were collected retrospectively through systematic review of hospital records. Demographic characteristics, relevant preoperative comorbidities, baseline laboratory investigations, operative characteristics, perioperative variables, and postoperative outcomes were recorded using a standardised data collection format. Preoperative variables included age, sex, relevant comorbid conditions, and baseline laboratory parameters. The baseline serum creatinine (SCr) value was obtained from the laboratory investigation performed closest to the date of surgery, preferably within 24 hours before the operative procedure. This preoperative SCr value was considered the baseline renal function measurement for subsequent assessment of postoperative changes. Intraoperative variables included the type of cardiac surgery, duration of cardiopulmonary bypass (CPB), aortic cross-clamp duration, and other relevant operative and hemodynamic parameters available from the medical records. Postoperative variables included serial SCr measurements, urine output, requirement for renal replacement therapy, duration of intensive care unit (ICU) stay, duration of hospital stay, and in-hospital mortality. Definition and Assessment of Acute Kidney Injury Postoperative AKI was defined and staged according to the Kidney Disease: Improving Global Outcomes (KDIGO) criteria [8]. AKI was considered present if any of the following criteria were fulfilled: an increase in SCr by ≥0.3 mg/dL (≥26.5 μmol/L) within 48 hours, an increase in SCr to ≥1.5 times the baseline value within 7 days, or a urine output of <0.5 mL/kg/h for at least 6 hours. The severity of AKI was classified into three stages according to the magnitude of increase in SCr and reduction in urine output. Stage 1 was defined as an increase in SCr to 1.5–1.9 times baseline or an increase of ≥0.3 mg/dL, or urine output <0.5 mL/kg/h for 6–12 hours. Stage 2 was defined as an increase in SCr to 2.0–2.9 times baseline or urine output <0.5 mL/kg/h for ≥12 hours. Stage 3 was defined as an increase in SCr to ≥3 times baseline, an increase in SCr to ≥4.0 mg/dL, initiation of renal replacement therapy, or urine output <0.3 mL/kg/h for ≥24 hours or anuria for ≥12 hours. For the purpose of the present study, patients were initially classified into two groups: those who developed postoperative AKI and those who did not. Patients who developed AKI were further categorised according to KDIGO stage to evaluate the severity of postoperative renal dysfunction. Outcome Measures The primary outcome of the study was the development of postoperative AKI following cardiac surgery. Secondary outcomes included the severity of AKI according to KDIGO staging, requirement for renal replacement therapy, postoperative ICU and hospital stay, and in-hospital mortality. The study also evaluated the association between postoperative AKI and relevant demographic, preoperative, intraoperative, and postoperative variables to evaluate factors associated with the development of postoperative AKI. Statistical Analysis Statistical analysis was performed using IBM SPSS Statistics, version 25.0 (IBM Corp., Armonk, NY, USA). Continuous variables were assessed for normality using the Shapiro–Wilk test and are presented as mean ± standard deviation (SD) for normally distributed data or median with interquartile range (IQR) for non-normally distributed data. Categorical variables are expressed as frequencies and percentages. Patients were categorized into AKI and non-AKI groups according to the KDIGO criteria. Continuous variables were compared between the two groups using the independent-samples t-test for normally distributed data or the Mann–Whitney U test for non-normally distributed data. Categorical variables were compared using the Pearson chi-square (χ²) test or Fisher’s exact test, as appropriate. Variables considered clinically relevant and those demonstrating an association at P<0.10 in univariate comparisons were considered for inclusion in the multivariable logistic regression model to identify factors independently associated with postoperative AKI. Results of regression analyses are reported as odds ratios (ORs) with 95% confidence intervals (CIs). Multicollinearity among candidate variables was assessed before multivariable modelling. All statistical tests were two-sided, and a P-value <0.05 was considered statistically significant.

A total of 100 patients undergoing elective cardiac surgery were included in the study. Of these, 62 (62.0%) were male, and 38 (38.0%) were female. The median age of the study population was 58 years (IQR: 46–65), and the median body mass index was 26.1 kg/m² (IQR: 23.6–29.8). Diabetes mellitus and hypertension were present in 51.0% and 57.0% of patients, respectively, while 69.0% had ischemic heart disease. Pre-existing chronic kidney disease was documented in 8.0% of patients. The median preoperative serum creatinine was 0.94 mg/dL (IQR: 0.78–1.16), median haemoglobin was 11.8 g/dL (IQR: 10.2–13.1), and median estimated glomerular filtration rate (eGFR) was 84 mL/min/1.73 m² (IQR: 68–96). The median left ventricular ejection fraction (LVEF) was 52% (IQR: 45–58), with 12.0% of patients having an LVEF below 40% (Table 1). Regarding operative characteristics, 70 (70.0%) patients underwent coronary artery bypass grafting (CABG) and 30 (30.0%) underwent valve replacement or repair. The median cardiopulmonary bypass (CPB) duration was 82 minutes (IQR: 68–106), while the median aortic cross-clamp time was 56 minutes (IQR: 43–71). Intraoperative blood product transfusion was required in 40.0% of patients, and 42.0% required postoperative inotropic or vasopressor support. Postoperative AKI developed in 28 (28.0%) patients, whereas 72 (72.0%) did not develop AKI. According to KDIGO staging, 17 (17.0%) patients had stage 1, 7 (7.0%) had stage 2, and 4 (4.0%) had stage 3 AKI. Thus, among the 28 patients who developed AKI, 60.7% had stage 1, 25.0% had stage 2, and 14.3% had stage 3 AKI (Figure 1). Renal replacement therapy was required in 3 (3.0%) patients. The median ICU and hospital stays were 5 days (IQR: 3–8) and 10 days (IQR: 8–14), respectively. Overall in-hospital mortality was 3.0% (Table 2). Comparison between patients with and without postoperative AKI demonstrated several significant differences. Patients who developed AKI were significantly older than those without AKI, with a median age of 64 years (IQR: 54–70) versus 56 years (IQR: 45–63; P=0.006). There were no statistically significant differences between the groups with respect to sex, BMI, diabetes mellitus, hypertension, ischemic heart disease, or congestive heart failure (all P>0.05). However, pre-existing chronic kidney disease was significantly more frequent among patients who developed AKI (17.9% vs. 4.2%; P=0.037). Preoperative renal and haematological parameters also differed significantly between the groups. Patients with AKI had a significantly lower median preoperative haemoglobin level than those without AKI (10.6 vs. 12.2 g/dL; P=0.002) and a higher median preoperative serum creatinine (1.12 vs. 0.89 mg/dL; P=0.003). Median eGFR was significantly lower in the AKI group (68 vs. 88 mL/min/1.73 m²; P=0.002). Similarly, median LVEF was lower among patients who developed AKI (47% vs. 53%; P=0.018). The type of cardiac surgery was not significantly associated with postoperative AKI (P=0.771). CABG was performed in 67.9% of patients who developed AKI compared with 70.8% of those without AKI, while valve surgery was performed in 32.1% and 29.2%, respectively. Patients who developed AKI had significantly longer CPB duration (101 vs. 75 minutes; P<0.001) and aortic cross-clamp duration (69 vs. 50 minutes; P<0.001). Intraoperative blood product transfusion was more frequent among patients with AKI (67.9% vs. 29.2%; P<0.001), as was the requirement for postoperative inotropic or vasopressor support (82.1% vs. 26.4%; P<0.001) (Table 3 and Figure 2). Postoperative clinical outcomes were significantly poorer among patients who developed AKI. The median ICU stay was 8 days (IQR: 5–11) in the AKI group compared with 4 days (IQR: 3–6) in the non-AKI group (P<0.001). Similarly, median hospital stay was significantly longer among patients with AKI (14 vs. 9 days; P<0.001). All three in-hospital deaths occurred among patients who developed AKI, corresponding to mortality rates of 10.7% in the AKI group and 0% in the non-AKI group (P=0.020). In the multivariable logistic regression analysis, several factors remained independently associated with postoperative AKI. Increasing age was associated with higher odds of AKI (adjusted OR [aOR] 1.05 per year; 95% CI: 1.01–1.10; P=0.021). Higher preoperative haemoglobin demonstrated a protective association (aOR 0.68 per 1 g/dL increase; 95% CI: 0.50–0.92; P=0.013), whereas increasing preoperative serum creatinine was associated with increased AKI risk (aOR 1.18 per 0.1 mg/dL increase; 95% CI: 1.03–1.36; P=0.019). Longer CPB duration (aOR 1.24 per 10-minute increase; 95% CI: 1.05–1.46; P=0.011) and longer aortic cross-clamp duration (aOR 1.29 per 10-minute increase; 95% CI: 1.06–1.58; P=0.012) were also independently associated with postoperative AKI. In addition, patients requiring intraoperative blood product transfusion had approximately 2.7-fold higher odds of developing postoperative AKI (aOR 2.71; 95% CI: 1.03–7.14; P=0.044). The strongest association was observed with postoperative inotropic or vasopressor support, which was associated with more than fourfold higher odds of AKI (aOR 4.38; 95% CI: 1.52–12.64; P=0.006) (Table 4 and Figure 3). Table 1. Preoperative Characteristics of the Study Population (N = 100) Patient characteristics Data, n (%) or Median (IQR) Male 62 (62.0) Female 38 (38.0) Age (years) 58 (46–65) BMI (kg/m²) 26.1 (23.6–29.8) Diabetes mellitus 51 (51.0) Hypertension 57 (57.0) Ischemic heart disease 69 (69.0) Smoking (current or ex-smoker) 31 (31.0) Previous cerebrovascular event 7 (7.0) Congestive heart failure 6 (6.0) Dyslipidemia 42 (42.0) Pre-existing chronic kidney disease 8 (8.0) Serum creatinine (mg/dL) 0.94 (0.78–1.16) Blood urea (mg/dL) 32 (25–43) Haemoglobin (g/dL) 11.8 (10.2–13.1) eGFR (mL/min/1.73 m²) 84 (68–96) LVEF (%) 52 (45–58) LVEF <40% 12 (12.0) [BMI: body mass index; eGFR: estimated glomerular filtration rate; IQR: interquartile range; LVEF: left ventricular ejection fraction.] Table 2. Operative and Postoperative Characteristics of the Study Population (N = 100) Characteristics Data, n (%) or Median (IQR) Type of surgery CABG 70 (70.0) Valve replacement/repair 30 (30.0) Cardiopulmonary bypass time (min) 82 (68–106) Aortic cross-clamp time (min) 56 (43–71) Intraoperative blood product transfusion 40 (40.0) Postoperative inotropic/vasopressor support 42 (42.0) Postoperative AKI 28 (28.0) No AKI 72 (72.0) KDIGO stage among total population Stage 1 17 (17.0) Stage 2 7 (7.0) Stage 3 4 (4.0) Renal replacement therapy/dialysis 3 (3.0) ICU stay (days) 5 (3–8) Hospital stay (days) 10 (8–14) In-hospital mortality 3 (3.0) [CABG: coronary artery bypass grafting; AKI: acute kidney injury; KDIGO: Kidney Disease: Improving Global Outcomes; ICU: intensive care unit; IQR: interquartile range.]. Table 3. Comparison of Clinical and Perioperative Characteristics Between AKI and Non-AKI Groups Variables AKI (n = 28) Non-AKI (n = 72) P-value Age (years) 64 (54–70) 56 (45–63) 0.006 Male sex 19 (67.9) 43 (59.7) 0.451 BMI (kg/m²) 26.5 (24.1–30.2) 25.9 (23.4-29.5) 0.418 Diabetes mellitus 16 (57.1) 35 (48.6) 0.444 Hypertension 18 (64.3) 39 (54.2) 0.361 Ischemic heart disease 21 (75.0) 48 (66.7) 0.420 Congestive heart failure 3 (10.7) 3 (4.2) 0.341 Pre-existing CKD 5 (17.9) 3 (4.2) 0.037 Preoperative haemoglobin (g/dL) 10.6 (9.5-11.9) 12.2 (10.8-13.3) 0.002 Preoperative creatinine (mg/dL) 1.12 (0.91-1.38) 0.89 (0.75-1.07) 0.003 eGFR (mL/min/1.73 m²) 68 (55–83) 88 (73–98) 0.002 LVEF (%) 47 (40–55) 53 (47–59) 0.018 Type of surgery 0.771 CABG 19 (67.9) 51 (70.8) Valve surgery 9 (32.1) 21 (29.2) CPB time (min) 101 (84–120) 75 (64–92) <0.001 Cross-clamp time (min) 69 (57–91) 50 (39–62) <0.001 Blood product transfusion 19 (67.9) 21 (29.2) <0.001 Postoperative inotropic/vasopressor support 23 (82.1) 19 (26.4) <0.001 ICU stay (days) 8 (5–11) 4 (3–6) <0.001 Hospital stay (days) 14 (10–18) 9 (7–12) <0.001 In-hospital mortality 3 (10.7) 0 (0.0) 0.020 [Data are presented as n (%) or median (IQR). AKI: acute kidney injury; BMI: body mass index; CKD: chronic kidney disease; eGFR: estimated glomerular filtration rate; LVEF: left ventricular ejection fraction; CABG: coronary artery bypass grafting; CPB: cardiopulmonary bypass; ICU: intensive care unit.] Table 4. Multivariable Logistic Regression Analysis of Factors Independently Associated with Postoperative AKI Predictor variable Adjusted OR 95% CI P-value Age (per 1-year increase) 1.05 1.01–1.10 0.021 Preoperative haemoglobin (per 1 g/dL increase) 0.68 0.50–0.92 0.013 Preoperative serum creatinine (per 0.1 mg/dL increase) 1.18 1.03–1.36 0.019 Cardiopulmonary bypass time (per 10-min increase) 1.24 1.05–1.46 0.011 Aortic cross-clamp time (per 10-min increase) 1.29 1.06–1.58 0.012 Intraoperative blood product transfusion 2.71 1.03–7.14 0.044 Postoperative inotropic/vasopressor support 4.38 1.52–12.64 0.006

The present study evaluated the incidence, perioperative risk factors, and short-term clinical consequences of postoperative acute kidney injury following elective cardiac surgery. AKI occurred in 28.0% of patients, and the majority of affected patients had KDIGO stage 1 disease. Advanced age, lower preoperative haemoglobin, higher baseline serum creatinine, prolonged cardiopulmonary bypass (CPB) and aortic cross-clamp durations, intraoperative blood product transfusion, and postoperative inotropic/vasopressor support were independently associated with AKI. Patients who developed AKI also experienced significantly longer ICU and hospital stays and greater in-hospital mortality. These findings reinforce the multifactorial pathogenesis of cardiac surgery-associated AKI, in which pre-existing susceptibility interacts with operative and postoperative haemodynamic and inflammatory insults [1,3,5]. The incidence of postoperative AKI in our study was 28.0%, which is almost identical to the 27.5% reported by Mohrag et al. [7]. In both studies, most cases were classified as KDIGO stage 1, indicating that mild renal dysfunction represents the most frequent presentation following cardiac surgery. Parolari et al. also demonstrated that AKI remains a frequent complication after adult cardiac surgery and emphasised the contribution of perioperative factors to its development [9]. Lagny et al. reported substantial variability in AKI incidence according to the diagnostic classification applied, highlighting the influence of case definition on reported rates [10]. Karkouti et al. likewise demonstrated a considerable burden of postoperative AKI and emphasised the importance of modifiable perioperative risk factors [11]. The close agreement between our findings and these reports supports the relevance of standardised KDIGO-based surveillance after cardiac surgery [8]. Renal replacement therapy was required in 3.0% of patients in the present study, closely comparable with the 2.4% dialysis requirement reported by Mohrag et al. [7]. Although severe AKI requiring dialysis occurred in only a minority of patients, its clinical implications are substantial because severe renal dysfunction is associated with prolonged hospitalisation, increased resource utilisation, and higher mortality [2,4]. The overall proportion requiring dialysis in our cohort is also consistent with the approximate 3% rate reported in the cardiac surgical literature [3]. Increasing age was independently associated with postoperative AKI in the present study. Patients who developed AKI were older than those who did not, and each additional year of age was associated with higher odds of renal injury. Mohrag et al. similarly identified older age as an independent predictor of postoperative AKI [7]. Advancing age is accompanied by a reduction in nephron mass and renal functional reserve, vascular stiffness, and impaired autoregulatory capacity, which may decrease tolerance to perioperative hypotension, inflammation, and ischemia. Baseline renal dysfunction showed a similar relationship in our study. Patients with AKI had higher preoperative serum creatinine, lower eGFR, and a higher frequency of pre-existing chronic kidney disease. Elevated baseline creatinine also remained independently associated with postoperative AKI. These findings parallel those of Mohrag et al. [7] and support previous evidence that impaired renal reserve is an important preoperative determinant of susceptibility to cardiac surgery-associated renal injury [3,5]. A particularly important finding was the association between lower preoperative haemoglobin and postoperative AKI. The AKI group had substantially lower haemoglobin levels, and increasing haemoglobin demonstrated an independent protective association. Mohrag et al. similarly identified preoperative anaemia as one of the strongest factors associated with postoperative AKI [7]. Reduced haemoglobin may decrease renal oxygen delivery, particularly within the relatively hypoxic renal medulla, and this effect may become more pronounced during CPB-induced haemodilution and perioperative hypoperfusion. The interaction between anaemia, transfusion requirement, and tissue oxygen delivery is clinically important. Ducrocq et al., in the REALITY randomised clinical trial, demonstrated the importance of carefully balancing restrictive and liberal blood transfusion strategies in anaemic cardiovascular patients [12], although their population differed from cardiac surgical patients. Mohrag et al. additionally considered haemoglobinopathy-related mechanisms in explaining severe preoperative anaemia within their Saudi Arabian population. Jastaniah described the epidemiological burden of sickle-cell disease in Saudi Arabia [13], while Alhuthali et al. documented important molecular patterns of alpha-thalassaemia within the same population [14]. These population-specific observations cannot be directly extrapolated to our patients from Bihar because haemoglobinopathy status was not assessed in the present study. Nevertheless, the biological mechanisms described in the related literature remain relevant. Crawford et al. discussed the challenges of cardiac surgery in patients with sickle-cell disease [15], while Khan et al. highlighted the potential renal and systemic complications associated with sickle-cell trait [16]. Raut et al. described specific perioperative concerns during cardiopulmonary bypass in patients with sickling disorders, including hypoxia, hypothermia, acidosis, and low-flow states [17]. Furthermore, Hu et al. demonstrated that an increased free haemoglobin ratio was associated with AKI after on-pump cardiac surgery [18]. Collectively, these observations provide mechanistic support for the potential roles of impaired oxygen delivery, haemolysis, oxidative stress, and microvascular injury in postoperative renal dysfunction, without implying that haemoglobinopathy was responsible for anaemia in our cohort. Diabetes mellitus and hypertension were common among our patients but were not significantly different between the AKI and non-AKI groups. This finding closely reproduces the observations of Mohrag et al., who likewise found no significant difference in diabetes or hypertension between patients with and without AKI [7]. However, the literature regarding diabetes is heterogeneous. Rodriguez-Quintero et al. reported that elevated glycosylated haemoglobin was associated with severe AKI following CABG [19], while Oezkur et al. demonstrated an association between chronic hyperglycaemia and postoperative AKI in patients undergoing coronary artery bypass surgery [20]. Wang et al. also reported an adverse association between diabetes mellitus and AKI after CABG [21]. Conversely, Moschopoulou et al. found that diabetes mellitus did not independently influence the incidence of AKI following cardiac surgery [22]. Kwon et al. similarly emphasized the importance of multiple interacting clinical and operative predictors rather than a single metabolic comorbidity in determining AKI risk following on-pump CABG [23]. The absence of a significant association in our cohort may therefore reflect the multifactorial nature of AKI and the relatively high background prevalence of diabetes and hypertension. In the present study, the type of cardiac surgery was not significantly associated with postoperative AKI. The proportions of patients undergoing CABG and valve surgery were comparable between the AKI and non-AKI groups. This suggests that the development of postoperative renal injury may be influenced more strongly by patient-related susceptibility and specific perioperative exposures than by the broad category of cardiac surgical procedure itself. Previous studies have demonstrated that procedure-related factors contribute to postoperative renal risk, particularly through differences in cardiopulmonary bypass duration, aortic cross-clamp time, blood loss, transfusion requirements, and perioperative haemodynamic instability [24,25]. Prolonged CPB and aortic cross-clamp times were among the strongest operative factors associated with AKI in our study. Patients who developed AKI had significantly longer CPB duration than those without AKI, and each 10-minute increase in CPB time independently increased the odds of AKI. Similarly, aortic cross-clamp duration was significantly longer among AKI patients and remained independently associated with renal injury. These findings closely correspond to those of Mohrag et al., who reported markedly longer CPB and cross-clamp durations among patients developing AKI, with cross-clamp time retaining significance in regression analysis [7]. Prolonged CPB exposes the kidneys to non-pulsatile blood flow, haemodilution, systemic inflammation, oxidative stress, microembolisation, and periods of reduced renal perfusion, whereas prolonged cross-clamping may further exacerbate systemic ischemia-reperfusion injury [1,5,9]. These observations suggest that minimization of avoidable CPB and myocardial ischemic times may form an important component of perioperative renal protection. Intraoperative blood product transfusion was significantly more frequent in patients with AKI and remained independently associated with approximately 2.7-fold higher odds of postoperative renal injury. Mohrag et al. similarly demonstrated a strong univariable association between blood product transfusion and AKI [7]. Karkouti et al. also identified transfusion among potentially modifiable perioperative factors associated with cardiac surgery-related AKI [11]. Blood transfusion may partly represent a marker of operative complexity, haemorrhage, and anaemia; however, biological effects related to storage lesions, inflammatory activation, altered erythrocyte deformability, and release of cell-free haemoglobin may additionally contribute to renal oxidative injury [18]. These findings support judicious use of blood products while maintaining adequate tissue oxygen delivery. Postoperative inotropic or vasopressor support demonstrated the strongest independent association with AKI in our study, increasing the odds of postoperative renal injury more than fourfold. This finding is highly consistent with Mohrag et al., in whom postoperative inotrope requirement remained strongly significant after logistic regression [7]. The need for inotropes or vasopressors likely identifies patients with impaired cardiac output, systemic haemodynamic instability, or persistent tissue hypoperfusion. Consequently, the association may not represent a direct nephrotoxic effect of these agents alone but rather the severity of the underlying circulatory disturbance. Maintenance of appropriate cardiac output, mean arterial pressure, intravascular volume, and renal perfusion therefore remains fundamental during the perioperative period. Other potentially important factors could also influence postoperative renal risk. Arora et al. reported that preoperative use of angiotensin-converting enzyme inhibitors or angiotensin receptor blockers was associated with an increased risk of AKI following cardiovascular surgery [26]. Zhang and Ma also evaluated the influence of preoperative ACE inhibitor therapy on outcomes following coronary artery bypass graft surgery [27]. In addition, Jiang et al. demonstrated that the interval between coronary angiography and cardiac surgery may influence AKI risk among patients with pre-existing renal dysfunction [28]. These exposures were not comprehensively available in our retrospective dataset and therefore could not be evaluated in the present analysis. Their potential influence should be considered when interpreting postoperative renal risk, particularly in patients with impaired baseline kidney function. Finally, postoperative AKI was associated with substantially poorer short-term outcomes. Patients who developed AKI had longer ICU stays and longer total hospitalisation, and all three in-hospital deaths occurred in the AKI group. These findings are consistent with Mohrag et al., who reported that all 30-day deaths in their cohort occurred among patients fulfilling AKI criteria [7]. Previous studies have similarly demonstrated that AKI following cardiac surgery is associated with increased short-term mortality, long-term mortality, and progression to chronic kidney disease [3,4]. Thus, even mild postoperative renal dysfunction should not be regarded as a transient biochemical abnormality. Early recognition of high-risk patients, optimisation of anaemia and baseline renal status, reduction of avoidable CPB and cross-clamp duration, judicious blood product utilisation, and meticulous postoperative haemodynamic management may collectively help reduce the occurrence and clinical consequences of cardiac surgery-associated AKI. Limitations of the Study: The present study has certain limitations that should be considered while interpreting the findings. First, its retrospective and single-centre design may limit the generalisability of the results and is inherently dependent on the completeness and accuracy of routinely recorded clinical data. Second, the relatively small sample size and limited number of postoperative AKI events may have reduced the statistical power for detecting weaker associations and may have constrained the stability of the multivariable logistic regression model. Therefore, the identified independent associations should be interpreted as exploratory and require validation in larger prospective cohorts. Third, some potentially relevant perioperative factors, including detailed intraoperative haemodynamic changes, fluid balance, nephrotoxic drug exposure, vasopressor doses, and other potentially modifiable renal risk factors, could not be comprehensively evaluated because of the retrospective nature of data collection. Finally, the study assessed only in-hospital outcomes; long-term renal recovery, progression to chronic kidney disease, readmission, and long-term mortality were not evaluated. Larger prospective multicentre studies with adequate sample sizes and longer follow-up are warranted to validate these findings and better define predictors of cardiac surgery-associated AKI.

Postoperative acute kidney injury was a common complication following cardiac surgery, occurring in more than one-quarter of patients and being associated with prolonged ICU and hospital stay and increased in-hospital mortality. Advanced age, lower preoperative haemoglobin, higher baseline serum creatinine, prolonged cardiopulmonary bypass and aortic cross-clamp times, blood product transfusion, and postoperative inotropic/vasopressor support were independently associated with postoperative AKI. Early identification of high-risk patients, careful perioperative renal monitoring, and optimisation of modifiable risk factors may help reduce the occurrence and adverse consequences of postoperative AKI.

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