Comment on “The impact of preoperative comorbidity and intraoperative hypotension on postoperative acute kidney injury after non-cardiac surgery: a structural equation modeling-based mediation analysis”

Dear Editor,

We read with interest the recent article by Jo et al. [1] on the mediating role of intraoperative hypotension (IOH) in the association between preoperative comorbidity and postoperative acute kidney injury (AKI). The use of structural equation modeling (SEM), provides useful mechanistic insight but there are some other issues. The use of SEM may highlight its mechanistic insight; however, further methodological and clinical relevance should be discussed.

Firstly, the use of American Society of Anesthesiologists physical status (ASA-PS) only for comorbidity burden may result in construct imprecision. The ASA-PS has a subjective character and does not provide detail on disease severity or organ dysfunction. Previous evidence indicates that quantitative physiologic markers (e.g., perfusion index), both manifest independently associated with postoperative AKI and are objective measures of the microcirculation status [2]. Including objective indices may improve exposure characterization.

Secondly, it is assumed that the hemodynamic susceptibility is comparable in all human beings. Recent data have shown that the management guided by hypotension prediction index (HPI), which allows for a proactive and individualized management of hemodynamics, markedly reduces IOH compared to standard care [3]. The discovery shows that low mean arterial pressure (MAP) thresholds (e.g., MAP < 60 mmHg) do not take into account differences in patients’ autoregulatory capacity and hemodynamic response.

Thirdly, AKI was treated as a binary or staged outcome post-operatively regardless of its prognostic heterogeneity. Clinical studies performed on certain surgical populations, including hepatic resection, AKI affecting the postoperative period correlates with adverse late onset outcomes [4]. Therefore, the prognosis of AKI is quite heterogeneous. The prognostic impact can vary depending on how you define the outcome of AKI treatment. This suggests that treating it as a static endpoint can mask clinically significant differences while also limiting the ability to interpret mediation pathways.

Lastly, the study did not account for larger preoperative data heterogeneity except for some laboratory variables. Recent evidence shows that having a non-anemic iron deficiency, even when conventional laboratory values are normal, is independently associated with an adverse postoperative outcome. This suggests that risk that is clinically relevant may be undetected if it is not part of the routine preoperative indicators [5]. According to this finding, some of the significant risk signals might not be captured by usual indicators. Therefore, there is a need for more detailed preoperative variables for better risk stratification and model validity.

In conclusion, although the current research adds to the knowledge of mediators of AKI, any future research should include objective physiological measurements, individualized hemodynamic targets, wider biochemical profiling and temporally resolved outcomes to strengthen causal inference and clinical applicability. We offer recommendations to enhance what is already an excellent article and look forward to future enlightening contributions from these investigators.