Postoperative acute kidney injury and serum creatinine: still central, still limited

Ah-Reum Cho

doi:10.4266/acc.001144

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Editorial Surgery Postoperative acute kidney injury and serum creatinine: still central, still limited: Acute and Critical Care 2026;41(1):183-185.
DOI: https://doi.org/10.4266/acc.001144
Published online: February 27, 2026

Ah-Reum Cho^1,2

¹Department of Anesthesia and Pain Medicine, Medical Research Institute, Pusan National University Hospital, Busan, Korea

²Department of Anesthesia and Pain Medicine, Pusan National University School of Medicine, Yangsan, Korea

Corresponding author: Ah-Reum Cho Department of Anesthesia and Pain Medicine, Pusan National University School of Medicine, 179 Gudeok-ro, Seo-gu, Busan 49241, Korea Tel: +82-51-240-7399 Fax: +82-51-242-7466 Email: archo@pusan.ac.kr

• Received: February 10, 2026 • Revised: February 22, 2026 • Accepted: February 23, 2026

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Postoperative acute kidney injury (AKI) remains one of the most common and prognostically significant complications after major surgery, particularly in emergency settings. Its occurrence is consistently associated with increased mortality, prolonged intensive care unit stays, and higher healthcare costs [1,2]. Despite this substantial clinical burden, postoperative AKI continues to occupy an ambiguous position in perioperative medicine: it is readily recognized and widely feared, yet it is rarely meaningfully modified once detected.

In this of Acute and Critical Care, investigators examine the prognostic implications of preoperative serum creatinine elevation and early postoperative creatinine recovery in patients undergoing emergency surgery for bowel perforation or infarction, as reported in “Failure of early creatinine recovery predicts poor survival after emergency surgery for bowel perforation or infarction” [3]. By focusing on absolute creatinine values and their early postoperative trajectories, the study demonstrates that failure of creatinine recovery by postoperative day 3 is strongly associated with major complications and short-term mortality. These findings reinforce a well-established observation in surgical critical care: patients with persistent postoperative renal dysfunction represent a particularly high-risk phenotype.

What this study offers is not a novel biomarker or a new diagnostic framework, but rather a pragmatic reflection of everyday clinical practice. In emergency surgical settings, application of the full Kidney Disease: Improving Global Outcomes criteria is often impractical. Baseline creatinine values may be unavailable, urine output data are frequently incomplete, and clinical decisions must be made under considerable time pressure [4]. Within these constraints, serum creatinine remains the most accessible and widely recognized indicator of renal function. Its enduring role reflects feasibility rather than diagnostic precision.

At the same time, the limitations of serum creatinine as a marker of AKI are well recognized. Creatinine is a functional marker that increases only after a substantial decline in glomerular filtration has already occurred [1]. Its concentration is influenced by age, sex, muscle mass, intravascular volume status, diet, and medications, which vary widely among critically ill surgical patients. Consequently, serum creatinine performs poorly as an early marker of renal injury and may fail to capture ongoing tubular damage or renal stress during the initial phase of the insult.

This duality—indispensable yet inadequate—defines the contemporary role of serum creatinine in postoperative AKI. Creatinine remains central to risk stratification not because it accurately reflects the onset or severity of kidney injury, but because no alternative marker has yet proven sufficiently actionable in routine clinical practice. Although stress and damage biomarkers have demonstrated prognostic promise, their adoption has been limited by cost, availability, and, critically, the absence of clearly defined management strategies triggered by their elevation [5]. Earlier detection alone does not improve outcomes if it does not lead to a change in management.

Earlier recognition of postoperative AKI, whether based on serum creatinine trajectories or emerging biomarkers, does not currently translate into targeted therapy. Care remains largely supportive, focusing on hemodynamic optimization, judicious fluid management, and avoidance of nephrotoxins [4,6]. Although these measures are essential components of perioperative care, they are neither specific to AKI nor uniquely initiated in response to its diagnosis. This limitation is reflected in contemporary AKI guidelines, which emphasize bundle-based approaches rather than discrete therapeutic interventions [4,6]. While such bundles appropriately acknowledge the multifactorial nature of AKI, they also underscore the absence of treatments that directly modify the course of established renal injury. Consequently, improvements in risk stratification tend to enhance prognostication more than they improve patient outcomes.

Within this context, early postoperative creatinine recovery is best interpreted as a prognostic checkpoint rather than an early diagnostic signal. Prior studies have demonstrated that delayed or absent renal recovery is associated with worse outcomes, even when traditional AKI severity thresholds are not exceeded [7,8]. Failure of creatinine to normalize by postoperative day 3 likely reflects unresolved systemic stress, such as persistent sepsis, inadequate source control, ongoing hypoperfusion, or microcirculatory dysfunction, rather than isolated renal pathology. Recognition of this pattern may justify closer monitoring, reassessment of surgical or hemodynamic adequacy, and earlier involvement of critical care or nephrology services; however, these responses remain indirect and address the broader clinical context rather than the kidney itself.

The study highlighted in this issue therefore illustrates both the utility and the limitations of serum creatinine in postoperative AKI. Creatinine dynamics can identify patients at exceptionally high risk and may serve as a practical signal to prompt heightened vigilance. However, they do not resolve the central challenge facing the field: how to link earlier and more precise detection of kidney injury to interventions that meaningfully improve outcomes.

Future progress in postoperative AKI will depend on bridging this gap. Biomarkers should be evaluated not only for predictive accuracy, but also for their capacity to guide therapies that improve patient-centered outcomes. Risk stratification tools should be embedded within care pathways that clearly define how management should differ once high-risk status is identified. Until such strategies are established, serum creatinine will remain what it is today: central to the assessment of postoperative AKI, yet inherently limited in what it can deliver. Thus, in postoperative AKI, the clinical value of creatinine lies less in early detection than in its ability to signal unresolved systemic stress and identify patients at persistently high risk.

NOTES

CONFLICT OF INTEREST

Ah-Reum Cho is an editorial board member of the journal but was not involved in the peer reviewer selection, evaluation, or decision process of this article. No other potential conflict of interest relevant to this article was reported.

FUNDING

None.

ACKNOWLEDGMENTS

None.

AUTHOR CONTRIBUTIONS

All the work was done by Ah-Reum Cho.

REFERENCES

1. Gameiro J, Fonseca JA, Neves M, Jorge S, Lopes JA. Acute kidney injury in major abdominal surgery: incidence, risk factors, pathogenesis and outcomes. Ann Intensive Care 2018;8:22.Article PubMed PMC PDF
2. Hoste EA, Kellum JA, Selby NM, Zarbock A, Palevsky PM, Bagshaw SM, et al. Global epidemiology and outcomes of acute kidney injury. Nat Rev Nephrol 2018;14:607-25.Article PubMed PDF
3. Kim HI, Lee MH, Jeon BJ, Yoon MK, Oh MK, Kim MG. Failure of early creatinine recovery predicts poor survival after emergency surgery for bowel perforation or infarction. Acute Crit Care 2026;41.Article PDF
4. Kidney Disease: Improving Global Outcomes (KDIGO) Group. KDIGO clinical practice guideline for acute kidney injury. Kidney Int Suppl 2012;2:1-138.
5. Rossiter A, La A, Koyner JL, Forni LG. New biomarkers in acute kidney injury. Crit Rev Clin Lab Sci 2024;61:23-44.Article PubMed
6. Ostermann M, Bellomo R, Burdmann EA, Doi K, Endre ZH, Goldstein SL, et al. Controversies in acute kidney injury: conclusions from a Kidney Disease: Improving Global Outcomes (KDIGO) Conference. Kidney Int 2020;98:294-309.Article PubMed PMC
7. Swaminathan M, Hudson CC, Phillips-Bute BG, Patel UD, Mathew JP, Newman MF, et al. Impact of early renal recovery on survival after cardiac surgery-associated acute kidney injury. Ann Thorac Surg 2010;89:1098-104.Article PubMed
8. Peerapornratana S, Fiorentino M, Priyanka P, Murugan R, Kellum JA. Recovery after AKI: effects on outcomes over 15 years. J Crit Care 2023;76:154280.Article PubMed PMC

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Postoperative acute kidney injury and serum creatinine: still central, still limited

Acute Crit Care. 2026;41(1):183-185. Published online February 27, 2026

DOI: https://doi.org/10.4266/acc.001144

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Postoperative acute kidney injury and serum creatinine: still central, still limited