Cardiorenal Syndrome Type 1 After Coronary Artery Bypass Grafting: Clinical and Metabolic Predictors of Acute Kidney Injury

Abstract Background Cardiorenal syndrome type 1 (CRS-1), characterised by acute cardiac dysfunction leading to acute kidney injury (AKI), represents a clinically important but under-recognised phenotype following coronary artery bypass grafting (CABG), where it significantly increases morbidity and mortality. Early risk stratification remains challenging due to the complex interplay between cardiac dysfunction and perioperative hemodynamic and metabolic disturbances. This study aimed to identify independent predictors of postoperative AKI, the majority of which occurred in the setting of CRS-1 after elective CABG. Methods This retrospective multicenter cohort study included 250 adult patients undergoing elective CABG across four tertiary cardiac centers. AKI was defined using Kidney Disease: Improving Global Outcomes (KDIGO) criteria. Preoperative, intraoperative, and early postoperative variables—including estimated glomerular filtration rate (eGFR), left ventricular ejection fraction (LVEF), intraoperative mean arterial pressure (MAP), serum lactate, and acid–base status—were extracted from electronic medical records. Multivariable logistic regression was used to identify independent predictors of postoperative AKI. Results Postoperative AKI occurred in 95 patients (38%), of whom 78 (82.1%) fulfilled the prespecified diagnostic criteria for cardiorenal syndrome type 1 (CRS-1). Independent predictors of AKI included preoperative eGFR < 60 mL/min/1.73 m² (adjusted odds ratio [aOR] 3.2; 95% CI 1.8–5.7; p < 0.001), LVEF < 40% (aOR 2.7; 95% CI 1.5–4.8; p = 0.002), intraoperative MAP < 65 mmHg sustained for > 20 minutes (aOR 2.9; 95% CI 1.6–5.2; p < 0.001), ICU admission serum lactate > 2.0 mmol/L (aOR 3.5; 95% CI 1.9–6.3; p < 0.001), metabolic acidosis with base excess < − 5 mmol/L (aOR 2.4; 95% CI 1.3–4.3; p = 0.004), CPB duration > 120 minutes (aOR 2.1; 95% CI 1.2–3.8; p = 0.011), and preoperative diabetes mellitus (aOR 1.9; 95% CI 1.1–3.4; p = 0.028). Patients with AKI experienced significantly higher in-hospital mortality (14.7% vs. 3.9%; p = 0.01) and prolonged intensive care unit length of stay (mean 7.8 vs. 3.9 days). Conclusions CRS-1-related AKI after CABG is driven by a multifactorial interaction between preoperative cardiac dysfunction, intraoperative hypotension, and early postoperative metabolic derangements. Integration of readily available clinical and metabolic parameters into perioperative monitoring may enable early risk stratification and timely initiation of cardio-renal protective strategies, thereby improving outcomes in high-risk patients.