CARDIAC SURGERY–ASSOCIATED ACUTE KIDNEY INJURY: FROM OXYGEN DELIVERY AND RENAL MEDULLARY HYPOXIA TO PRECISION CARDIORENAL MONITORING

Cardiac surgery–associated acute kidney injury (CSA-AKI) complicates 20–50% of procedures requiring car­diopulmonary bypass (CPB), independently increasing perioperative mortality threefold to fivefold, triggering pro­gression to chronic kidney disease (CKD) in 25–30% of surviving cohorts, and generating substantial long-term car­diovascular burden. This narrative review systematises the pathophysiology, biomarker landscape, and evidence-based preventive strategies of CSA-AKI, with emphasis on the critical threshold of indexed oxygen delivery (DO₂I) below 272 mL/min/m² inducing systemic dysoxia; ischaemia–reperfusion cascades and endothelial glycocalyx col­lapse; neutrophil gelatinase-associated lipocalin (NGAL) providing early structural signals within 2–6 hours post-CPB (AUC 0.78–0.85 in adults); [TIMP-2]×[IGFBP7] identifying G₁ cell-cycle arrest stress (AUC 0.80, SAPPHIRE trial); and preoperative urinary DKK3 reflecting baseline renal vulnerability (OR 5.27, Lancet 2019). Goal-directed perfusion maintaining DO₂I above 272 mL/min/m² significantly reduces CSA-AKI incidence (RR 0.71, 95% CI 0.56–0.90). Bi­omarker-guided KDIGO care bundle implementation was validated in PrevAKI RCTs. A structured literature search was conducted across PubMed, Scopus, and Web of Science (January 2005 – March 2026); 41 references verified by DOI or URL were selected from over 310 initially screened publications.