Interpreting perioperative oliguria during sevoflurane anesthesia: excretory physiology, fluid responsiveness, and renal endpoints.

Perioperative oliguria is a renal signal during anesthesia, but its automatic interpretation as acute kidney injury may misclassify renal endpoints in anesthetic research. The available evidence is strongest for sevoflurane rather than for volatile anesthetics as a homogeneous class. Small mechanistic and randomized clinical studies suggest that sevoflurane can reduce urine output and natriuresis and increase renin activity compared with propofol-based total intravenous anesthesia, consistent with renal sympathetic and renin-angiotensin-aldosterone system-mediated sodium and water retention. However, these excretory differences have not been consistently accompanied by parallel increases in tubular injury biomarkers or by uniform differences in creatinine-defined or patient-centered kidney outcomes. Therefore, sevoflurane-associated oliguria should be interpreted as a context-dependent renal signal rather than as either benign physiology or definite kidney injury. This narrative review proposes a layered approach that separates excretory physiology, creatinine-defined functional acute kidney injury, tubular stress or injury biomarkers, and patient-centered kidney outcomes. The framework is intended as an analytical aid, not as a validated diagnostic or treatment algorithm. Its practical implication is that oliguria during sevoflurane anesthesia should prompt reassessment of perfusion, venous congestion, anesthetic exposure, baseline kidney risk, and postoperative trajectory before reflexive fluid administration or automatic labeling as acute kidney injury.