Prognostic factors of sepsis following laparoscopic hiatal hernia repair

Abstract

BACKGROUND

Laparoscopic hiatal hernia repair (LHHR) is the surgical intervention of choice for symptomatic hiatal hernias; however, a major complication such as postoperative sepsis presents a serious challenge, particularly in elderly and comorbid patients. Acute kidney injury (AKI) occurring in patients with sepsis is termed sepsis-associated AKI. This complication has been reported to affect 40%–50% of intensive care unit patients with sepsis and is an independent risk factor for increased mortality and prolonged hospital stay. A large proportion of patients who develop sepsis after LHHR may subsequently develop AKI, but the incidence, predictors, and prognosis of AKI remain mostly unknown in this setting despite the clinical importance of this complication. The objective of this study was to identify independent prognostic factors and examine the AKI-mortality association in a surgical cohort.

AIM

To evaluate the prognostic factors associated with postoperative sepsis following LHHR, with particular emphasis on the incidence, risk factors, and clinical impact of AKI in this patient population. The primary objectives were to determine perioperative predictors of sepsis severity, assess AKI as an independent prognostic determinant, and establish evidence-based recommendations for postoperative monitoring and management strategies.

METHODS

We conducted a retrospective analysis of 214 patients who underwent LHHR at the Department of Gastrointestinal Surgery between January 2019 and December 2024. Patients who developed sepsis within 30 days of surgery were identified and compared with non-sepsis controls. Sepsis was defined according to the Sepsis-3 consensus criteria. AKI was diagnosed and staged using the Kidney Disease: Improving Global Outcomes criteria. Logistic regression analysis identified independent predictors of sepsis, AKI, and in-hospital mortality. Receiver operating characteristic curve analysis evaluated the discriminative capacity of identified predictors, and Kaplan–Meier curves compared survival outcomes between the AKI and non-AKI subgroups among patients with sepsis.

RESULTS

Of 214 patients, 42 (19.6%) developed postoperative sepsis. Among patients with sepsis, 18 (42.9%) were diagnosed with AKI: 7 (38.9%) with Kidney Disease: Improving Global Outcomes stage 1, 6 (33.3%) with stage 2, and 5 (27.8%) with stage 3. The overall in-hospital mortality rate among patients with sepsis was 16.7% (7/42); mortality was significantly higher in the AKI subgroup (38.9%, 7/18) than in the non-AKI subgroup (0.0%, P < 0.001). Independent predictors of sepsis included American Society of Anesthesiologists class ≥ III [odds ratio (OR) 3.42, 95% confidence interval (CI): 1.68–6.97, P = 0.001], operative time > 180 minutes (OR 2.85, 95%CI: 1.41–5.77, P = 0.003), and preoperative hypoalbuminemia (OR 2.61, 95%CI: 1.27–5.35, P = 0.009). Independent predictors of AKI among patients with sepsis included Sequential Organ Failure Assessment score ≥ 8 at sepsis onset (OR 4.73, 95%CI: 1.52–14.72, P = 0.007), vasopressor requirement (OR 3.86, 95%CI: 1.24–12.04, P = 0.020), and preoperative creatinine elevation (OR 3.14, 95%CI: 1.03–9.61, P = 0.044). AKI-stage progression was associated with incremental mortality (stage 1: 14.3%; stage 2: 33.3%; stage 3: 80.0%, P < 0.001).

CONCLUSION

Postoperative sepsis following LHHR carries significant morbidity, with AKI representing a critical determinant of prognosis. AKI stage correlates strongly with in-hospital mortality, and its early identification should guide intensified organ support and renal-protective strategies. Preoperative optimization of nutritional status and renal function, combined with vigilant postoperative sepsis monitoring, may mitigate these risks. Prospective multicenter studies are required to validate predictive scoring systems and evaluate targeted interventions for this high-risk cohort.

Key Words: Laparoscopic hiatal hernia repair; Postoperative sepsis; Acute kidney injury; Prognosis; Perioperative outcome; Organ dysfunction; Kidney Disease: Improving Global Outcomes criteria

Core Tip: Postoperative sepsis occurs in 19.6% of patients undergoing laparoscopic hiatal hernia repair, with acute kidney injury (AKI) complicating 42.9% of septic cases. All in-hospital deaths occurred in the AKI subgroup, with stage 3 AKI carrying 80.0% mortality. American Society of Anesthesiologists class ≥ III, operative time > 180 minutes, and preoperative hypoalbuminemia independently predict sepsis. Combined Sequential Organ Failure Assessment and Kidney Disease: Improving Global Outcomes staging achieves superior mortality discrimination (area under the curve 0.924). Early AKI recognition and preoperative nutritional optimization are critical for improving outcomes.

INTRODUCTION

Hiatal hernia is one of the most prevalent structural abnormalities of the upper gastrointestinal tract, estimated to affect 10%–80% of the adult population, with increasing prevalence in older and obese individuals[1]. Laparoscopic hiatal hernia repair (LHHR) is now the surgical standard of care for symptomatic and paraesophageal hernias, with several advantages over open approaches, including less blood loss, shorter hospitalization time, and quicker recovery[2]. Although the procedure itself is minimally invasive, postoperative complications continue to represent an important clinical challenge, occurring in 20%–30% of patients, especially in older or comorbid patients[3].

Sepsis is caused by an uncontrolled host response to infection and acute organ dysfunction and is one of the serious postoperative complications of abdominal surgery[4]. The incidence of postoperative sepsis after laparoscopic gastrointestinal surgery is reported to vary from 2%–20%, depending on patient, procedural, and institutional factors[5]. However, sepsis after LHHR may derive from a number of sources, such as esophageal or gastric perforation, pulmonary infection caused by aspiration, or wound infection, and its prompt identification is critical to optimize survival[6].

Acute kidney injury (AKI) is one of the most common and clinically important organ dysfunctions that occurs in the context of sepsis. In intensive care unit patients with sepsis, AKI is estimated to be present in 40%–50% of patients and is independently associated with prolonged mechanical ventilation, increased length of stay, requirement for renal replacement therapy, and hospital mortality[7]. Sepsis-associated AKI has a complex pathophysiology that encompasses microvascular dysfunction, inflammatory cytokine-mediated tubular injury, and impaired renal autoregulation, frequently in the context of underlying renal injury susceptibility[8]. Although AKI is increasingly recognized as a prognostic predictor, the clinical significance of AKI in sepsis for patients who have undergone LHHR remains incompletely defined.

The Sepsis-3 definition, proposed in 2016, redefined sepsis as life-threatening organ dysfunction due to a dysregulated response to infection and operationalized it using the Sequential Organ Failure Assessment (SOFA) score. At the same time, standardized Kidney Disease: Improving Global Outcomes (KDIGO) criteria have established common criteria to define and stage AKI, making risk stratification for prognosis feasible across diverse surgical and critical care populations[9]. Such frameworks may apply to the unique context of post-LHHR sepsis, whereby actionable predictors may be identified, offering guidance on therapeutic escalation.

To date, limited literature has examined AKI as a prognostic modifier of sepsis following LHHR, and the perioperative determinants of this complication remain incompletely characterized. Given that sepsis following major abdominal surgery is multifactorial, we performed a comprehensive analysis of perioperative clinical variables associated with the incidence, risk factors, and outcomes of sepsis and AKI in this population. This work aims to offer evidence-based guidance for preoperative risk stratification, postoperative surveillance, and organ-protective interventions based on independent prognostic determinants and a closer evaluation of the AKI–mortality relationship.

MATERIALS AND METHODS

Study design and patient selection

This retrospective study analyzed consecutive patients who underwent LHHR at the Department of Gastrointestinal Surgery between January 2019 and December 2024. The study protocol was reviewed and approved by the Ethics Committee of the Brain Hospital of Hunan Province (The Second People’s Hospital of Hunan Province), No. 2025K095. The requirement for informed consent was waived given the retrospective design.

The inclusion criteria were age ≥ 18 years, elective or semi-elective LHHR (types I–IV), complete perioperative records including laboratory data, postoperative follow-up of ≥ 30 days or documented in-hospital death, and availability of a preoperative creatinine measurement within 7 days of surgery.

The exclusion criteria were conversion to open surgery, pre-existing end-stage renal disease requiring chronic dialysis, pre-existing sepsis at the time of surgery, concurrent malignancy, emergent procedures, incomplete clinical or laboratory data, and perioperative immunosuppressive therapy for indications other than standard stress-dose steroids.

Definitions

Postoperative sepsis was defined according to the Sepsis-3 criteria as a suspected or confirmed infection with an acute SOFA score increase of ≥ 2 points from baseline, occurring within 30 days of surgery. Septic shock was defined as sepsis requiring vasopressor therapy to maintain a mean arterial pressure ≥ 65 mmHg and a serum lactate level > 2 mmol/L in the absence of hypovolemia. AKI was diagnosed and staged according to the KDIGO 2012 guidelines: Stage 1, serum creatinine increase ≥ 0.3 mg/dL within 48 hours or 1.5–1.9 × baseline within 7 days; stage 2, 2.0–2.9 × baseline; and stage 3, ≥ 3.0 × baseline, creatinine ≥ 4.0 mg/dL, or initiation of renal replacement therapy. Hypoalbuminemia was defined as a preoperative serum albumin level < 35 g/L.

Statistical analysis

Statistical analyses were performed using SPSS 26.0 (IBM Corp., Armonk, NY, United States) and R version 4.3.0. Continuous variables were expressed as mean ± SD or median (interquartile range). Categorical variables were presented as n (%). Between-group comparisons were performed using the independent-samples t-test or Mann–Whitney U test for continuous variables and the χ² or Fisher’s exact test for categorical variables. Multivariable logistic regression analysis was used to identify independent predictors of sepsis and AKI, with variables with P < 0.10 in the univariate analysis included as candidates. Results were expressed as odds ratios (ORs) with 95% confidence intervals (CIs). Receiver operating characteristic curve analysis with DeLong’s method was used to compare discriminative performance. Kaplan–Meier survival curves were compared using the log-rank test. Statistical significance was set at P < 0.05 (2-tailed).

RESULTS

Patient characteristics

A total of 214 patients met the inclusion criteria. Among these, 42 (19.6%) developed postoperative sepsis within 30 days. Baseline characteristics are presented in Table 1. Patients with sepsis were significantly older (67.4 ± 10.3 years vs 59.8 ± 11.7 years, P = 0.001), had a higher American Society of Anesthesiologists (ASA) classification (P < 0.001), and had more frequent preoperative hypoalbuminemia (P = 0.004). The median time to sepsis onset was 4.0 days (interquartile range: 2.0–7.0) postoperatively. No significant difference was observed in hernia type distribution between the groups (P = 0.312).

Table 1 Baseline characteristics of the study population (n = 214).

Characteristic	Total (n = 214)	Sepsis (n = 42)	Non-sepsis (n = 172)
Age, years	62.1 ± 11.9	67.4 ± 10.3	59.8 ± 11.7
Female sex	128 (59.8)	23 (54.8)	105 (61.0)
BMI, kg/m2	28.4 ± 5.1	30.2 ± 5.8	27.9 ± 4.8
ASA class ≥ III	74 (34.6)	24 (57.1)	50 (29.1)
Hypoalbuminemia	46 (21.5)	16 (38.1)	30 (17.4)
Diabetes mellitus	58 (27.1)	16 (38.1)	42 (24.4)
Operative time, minutes	148 (112–196)	192 (151–247)	138 (106–178)
Hernia type IV	68 (31.8)	16 (38.1)	52 (30.2)
Preoperative creatinine, mg/dL	0.92 ± 0.31	1.08 ± 0.42	0.88 ± 0.27
SOFA score at sepsis onset	—	6.0 (4.0–9.0)	—

Data are presented as mean ± SD, n (%), or median (interquartile range).

ASA: American Society of Anesthesiologists; BMI: Body mass index; SOFA: Sequential Organ Failure Assessment.

Incidence and predictors of postoperative sepsis

Multivariable logistic regression identified 3 independent predictors of postoperative sepsis (Table 2): ASA class ≥ III (OR 3.42, 95%CI: 1.68–6.97, P = 0.001), operative time > 180 minutes (OR 2.85, 95%CI: 1.41–5.77, P = 0.003), and preoperative hypoalbuminemia (OR 2.61, 95%CI: 1.27–5.35, P = 0.009). The combined receiver operating characteristic model incorporating all 3 predictors yielded an area under the curve (AUC) of 0.812 (95%CI: 0.742–0.882), with a sensitivity of 76.2%, specificity of 74.4%, positive predictive value of 47.1%, and negative predictive value of 91.4% (Figure 1).

Figure 1 Receiver operating characteristic curves for independent predictors of postoperative sepsis. Receiver operating characteristic curves for the combined multivariable model (AUC = 0.812, 95% confidence interval: 0.742–0.882) and each individual independent predictor: ASA class ≥ III (AUC = 0.726), operative time > 180 minutes (AUC = 0.698), and preoperative hypoalbuminemia (AUC = 0.672). The diagonal dashed line represents the reference classifier (AUC = 0.500). The combined model demonstrated a sensitivity of 76.2%, specificity of 74.4%, positive predictive value of 47.1%, and negative predictive value of 91.4%. ASA: American Society of Anesthesiologists; AUC: Area under the curve.

Table 2 Multivariable predictors of postoperative sepsis.

Variable	OR	95%CI	P value
ASA class ≥ III	3.42	1.68–6.97	0.001
Operative time > 180 minutes	2.85	1.41–5.77	0.003
Preoperative hypoalbuminemia	2.61	1.27–5.35	0.009
Age ≥ 65 years	1.88	0.92–3.86	0.083
Diabetes mellitus	1.64	0.79–3.43	0.187
Hernia type IV	1.42	0.68–2.97	0.350

Reference categories: American Society of Anesthesiologists class I–II; operative time ≤ 180 minutes; albumin ≥ 35 g/L.

ASA: American Society of Anesthesiologists; CI: Confidence interval; OR: Odds ratio.

Incidence and staging of AKI among patients with sepsis

Among 42 patients with sepsis, 18 (42.9%) developed AKI at any stage. KDIGO staging revealed 7 patients (38.9%) at stage 1, 6 (33.3%) at stage 2, and 5 (27.8%) at stage 3. Among patients with AKI stage 3, 3 (60.0%) required renal replacement therapy (continuous veno-venous hemofiltration). The median time from sepsis diagnosis to AKI onset was 1.0 day (interquartile range: 0.5–2.0). The AKI stage distribution and associated outcomes are presented in Table 3 and Figure 2.

Figure 2 Clinical outcomes stratified by Kidney Disease: Improving Global Outcomes acute kidney injury stage among patients with sepsis (n = 42). Grouped bar chart comparing in-hospital mortality, ICU admission rate, and vasopressor requirement across 4 groups: No AKI (n = 24), AKI stage 1 (n = 7), AKI stage 2 (n = 6), and AKI stage 3 (n = 5). In-hospital mortality increased incrementally with AKI stage: 0.0%, 14.3%, 33.3%, and 80.0% for stages 0–3, respectively (P < 0.001). AKI: Acute kidney injury; ICU: Intensive care unit.

Table 3 Acute kidney injury stage distribution and associated outcomes among patients with sepsis (n = 42).

Parameter	No AKI (n = 24)	AKI stage 1 (n = 7)	AKI stage 2 (n = 6)	AKI stage 3 (n = 5)
In-hospital mortality	0 (0.0)	1 (14.3)	2 (33.3)	4 (80.0)
ICU admission	6 (25.0)	5 (71.4)	6 (100.0)	5 (100.0)
Vasopressor requirement	4 (16.7)	3 (42.9)	4 (66.7)	5 (100.0)
RRT required	0 (0.0)	0 (0.0)	0 (0.0)	3 (60.0)
ICU LOS, days		5.0 (3.0–7.0)	9.5 (7.0–13.0)	16.0 (10.0–22.0)
Hospital LOS, days	11.0 (8.0–15.0)	16.0 (12.0–21.0)	22.0 (17.0–31.0)	28.0 (19.0–41.0)

Data are presented as n (%) or median (interquartile range).

AKI: Acute kidney injury; ICU: Intensive care unit; LOS: Length of stay; RRT: Renal replacement therapy.

Predictors of AKI among patients with sepsis

Multivariable logistic regression within the septic cohort identified 3 independent predictors of AKI (Table 4): SOFA score ≥ 8 at sepsis onset (OR 4.73, 95%CI: 1.52–14.72, P = 0.007), vasopressor requirement (OR 3.86, 95%CI: 1.24–12.04, P = 0.020), and preoperative creatinine elevation above the normal reference range (OR 3.14, 95%CI: 1.03–9.61, P = 0.044). Age ≥ 70 years and diabetes mellitus showed borderline significance in the univariate analysis but did not achieve independent significance (P = 0.092 and P = 0.141, respectively) in the multivariable model.

Table 4 Independent predictors of acute kidney injury among patients with sepsis (n = 42).

Variable	OR	95%CI	P value
SOFA score ≥ 8 at sepsis onset	4.73	1.52–14.72	0.007
Vasopressor requirement	3.86	1.24–12.04	0.020
Elevated preoperative creatinine	3.14	1.03–9.61	0.044
Age ≥ 70 years	2.21	0.87–5.64	0.092
Diabetes mellitus	1.83	0.82–4.08	0.141

CI: Confidence interval; OR: Odds ratio; SOFA: Sequential Organ Failure Assessment.

Mortality and organ failure outcomes

Overall in-hospital mortality among patients with sepsis was 16.7% (7/42). All deaths occurred in the AKI subgroup, yielding an AKI-associated mortality of 38.9% (7/18) vs 0.0% (0/24) in the non-AKI sepsis subgroup (P < 0.001). Among non-surviving patients, 5 required renal replacement therapy, and 4 developed concurrent respiratory failure requiring mechanical ventilation (Figure 3). Table 5 presents a comparison of organ failure profiles between the AKI and non-AKI subgroups of patients with sepsis.

Figure 3 Kaplan–Meier in-hospital survival curves comparing patients with vs without acute kidney injury among patients with sepsis. Kaplan–Meier curves illustrate in-hospital survival probability over 30 days following sepsis diagnosis in patients with AKI (n = 18) vs without AKI (n = 24). All 7 in-hospital deaths occurred in the AKI subgroup (mortality 38.9% vs 0.0%). Numbers at risk at selected time points are shown below the x-axis. Log-rank test: P < 0.001. AKI: Acute kidney injury.

Table 5 Organ failure profile: Acute kidney injury vs non-acute kidney injury among patients with sepsis.

Organ failure parameter	AKI (n = 18)	Non-AKI (n = 24)
In-hospital mortality	7 (38.9)	0 (0.0)
Respiratory failure	10 (55.6)	5 (20.8)
Mechanical ventilation	8 (44.4)	2 (8.3)
Cardiovascular failure	12 (66.7)	4 (16.7)
Hepatic dysfunction	6 (33.3)	2 (8.3)
Peak SOFA score	10.5 (8.0–14.0)	5.0 (3.0–7.0)

Data are presented as n (%) or median (interquartile range).

AKI: Acute kidney injury; SOFA: Sequential Organ Failure Assessment.

Comparative diagnostic performance of prognostic scores

Table 6 summarizes the discriminative performance of established clinical scoring systems for predicting in-hospital mortality among patients with sepsis. The SOFA score at sepsis onset demonstrated the highest AUC among the individual scoring systems (0.891), followed by KDIGO AKI stage (AUC 0.864). The Acute Physiology and Chronic Health Evaluation II score at intensive care unit admission showed an AUC of 0.843. Combined SOFA + KDIGO staging achieved the highest discriminative performance, with an AUC of 0.924 (95%CI: 0.852–0.978, P < 0.001 vs SOFA alone).

Table 6 Discriminative performance of prognostic scoring systems for in-hospital mortality.

Scoring system	AUC	95%CI	Sensitivity (%)	Specificity (%)
SOFA score at onset	0.891	0.797–0.951	85.7	82.9
KDIGO AKI stage	0.864	0.764–0.933	100.0	72.7
APACHE II score	0.843	0.739–0.917	71.4	85.7
qSOFA score	0.742	0.629–0.836	71.4	71.4
Combined SOFA + KDIGO	0.924	0.852–0.978	100.0	82.9

AKI: Acute kidney injury; APACHE II: Acute Physiology and Chronic Health Evaluation II; AUC: Area under the curve; CI: Confidence interval; KDIGO: Kidney Disease: Improving Global Outcomes; qSOFA: Quick Sequential Organ Failure Assessment; SOFA: Sequential Organ Failure Assessment.

DISCUSSION

In this systematic investigation, we examined the incidence, predictors, and outcomes of postoperative sepsis after LHHR, with special attention to AKI as a prognostic modifier. The results of our study show that 1 in 5 patients undergoing LHHR developed postoperative sepsis and that AKI occurred in approximately 43% of patients with sepsis, with all in-hospital deaths confined to the AKI subgroup. This is, to our knowledge, one of the earliest studies to apply both Sepsis-3 and KDIGO criteria to phenotype organ dysfunction patterns in the postoperative LHHR context, providing a detailed mechanistic pathway linking sepsis with lethal outcomes.

Compared with estimates for laparoscopic cholecystectomy (2%–5%), the postoperative sepsis rate of 19.6% identified in our cohort is higher but comparable to the rates reported for anti-reflux procedures and complex hiatal hernia repair, especially paraesophageal hernia repair[10,11]. The frequency of type IV hernias in our cohort, which require extensive mediastinal dissection and are associated with an increased risk of esophagogastric injury and pleural contamination, may explain the higher rate. In addition, the cumulative impact of older age, a higher prevalence of ASA class ≥ III, comorbidities such as diabetes, and hypoalbuminemia in our cohort may have contributed to a heightened postoperative infectious risk because malnutrition is known to compromise immune function[12,13].

The fact that ASA class ≥ III emerged as the most powerful independent predictor of sepsis (OR 3.42) highlights the significant influence of baseline comorbidity burden on risk stratification in the postoperative setting. This observation is in keeping with the larger body of general surgical literature confirming ASA classification as a validated marker of physiological reserve and immune competence[14]. Long operative time (> 180 minutes), the second independent predictor (OR 2.85), probably encompasses an interaction between technical complexity and cumulative intraoperative physiological stress, including hypothermia, hypoperfusion, and anesthesia-mediated immune inhibition due to the prolonged duration of the procedure. Preoperative hypoalbuminemia (OR 2.61) is a widely recognized marker of protein-calorie malnutrition and immune dysfunction, which can compromise wound healing, mucosal barrier integrity, and antibody production[15]. Together, these 3 predictors characterize an at-risk phenotype in older patients with multimorbidity, nutritional depletion, and anatomically complex hernias, conditions in which preoperative optimization may critically influence postoperative courses.

The 42.9% AKI rate in patients with sepsis is comparable to rates reported in the general surgical sepsis literature[7], and our KDIGO stage distribution resembles that of population-based intensive care unit data indicating that higher-stage AKI disproportionately accounts for mortality[8]. AKI stage 3 had a mortality rate of 80.0% in our cohort, highlighting the clinical importance of early AKI recognition. SOFA score ≥ 8 and vasopressor requirement are independent AKI predictors, demonstrating the systemic impairment caused by sepsis and identifying patients who are at particularly high risk of developing AKI. Preoperative creatinine elevation was also an independent AKI predictor (OR 3.14), illustrating that subclinical renal impairment, frequently undetected in patients with adequate urine output and stable serum electrolytes, may substantially compromise the remaining renal reserve needed to withstand the hemodynamic and inflammatory insults of sepsis[9,16].

The contrasting mortality rates between the AKI and non-AKI subgroups (38.9% vs 0.0%) must be highlighted here. All patients in the non-AKI sepsis subgroup with systemic infection and organ dysfunction survived hospitalization. This differential survival likely reflects the centrality of renal function in systemic homeostasis. Given the kidney’s essential roles in volume regulation, electrolyte balance, acid–base homeostasis, and drug clearance, AKI may act both as a marker of systemic severity and an autonomous amplifier of organ crosstalk dysfunction[17]. The onset of kidney failure is followed by the accumulation of inflammatory mediators, uremic toxins, and fluid overload, leading to a vicious and self-reinforcing cycle of pulmonary, cardiac, and hepatic dysfunction. The higher rates of cardiovascular failure (66.7% vs 16.7%) and respiratory failure (55.6% vs 20.8%) in the AKI subgroup also corresponded with the concept of an organ interaction cascade in sepsis[18].

Our cohort had a high AUC for mortality with the combined SOFA + KDIGO model (0.924), which was significantly higher than that of either SOFA or KDIGO staging alone. This incremental discriminative value indicates that the renal staging system provides important prognostic information complementary to the overall SOFA score’s primary summary metric of organ dysfunction, presumably because KDIGO staging captures both the magnitude and sequence of renal dysfunction with greater granularity than does the simple classification inherent in renal SOFA subscores[4,9]. This has clear clinical relevance for intensivist management; SOFA score ≥ 8 and AKI stage ≥ 2 should prompt early referral to nephrology, preparation for renal replacement therapy, and vigorous fluid resuscitation, with attention focused on restoring renal perfusion pressure as early as possible[19,20].

Our finding of a median time from sepsis diagnosis to AKI onset of 1.0 day indicates that the development of this condition may occur within hours after sepsis recognition among the most vulnerable patients, affording only an exceedingly short window to institute potentially preventive measures. This finding supports the rationale for early postoperative near-patient monitoring of AKI biomarkers [especially urinary NGAL, urinary TIMP-2 × IGFBP7 (the basis of NephroCheck), and serum cystatin C] in high-risk patients[21]. These biomarkers have shown predictive superiority to serum creatinine for identifying AKI prior to glomerular filtration rate-based thresholds, thus opening the possibility of preemptive interventions, including hemodynamic optimization, nephrotoxic drug avoidance, and targeted fluid management, that can be used to prevent the progression of AKI[22].

Improvement of preoperative nutritional status is possibly one of the most actionable prophylactic measures derived from our data analyses. In randomized trials, preoperative nutritional intervention with enteral supplementation has been associated with a lower postoperative infection rate, shorter hospital stay, and reduced inflammatory response among patients undergoing gastrointestinal surgery[23]. The independent association between preoperative hypoalbuminemia and postoperative sepsis in our cohort supports the hypothesis that systematic preoperative albumin repletion, coupled with structured nutritional support ideally commencing 2–4 weeks before elective LHHR in patients with hypoalbuminemia, may serve as a potential target for modifying postoperative risk. Likewise, in the context of preoperative assessment of renal function beyond standard serum creatinine, the inclusion of estimated glomerular filtration rate and urine albumin–creatinine ratio would permit improved identification of patients with pre-existing chronic kidney disease who require heightened perioperative renal protection[24,25].

There are several limitations of this study that need to be acknowledged. First, the retrospective, single-center study design limits generalizability and may have introduced selection and information bias. Second, although the sample size was sufficient for the primary analyses, statistical power was limited for subgroup analyses, especially within the AKI stage 3 subgroup (n = 5). Third, cause-specific mortality data were available for only a subset of patients; thus, it could not be determined whether death was directly attributable to AKI vs sepsis-related multiorgan failure. Fourth, postoperative fluid balance data, the type and duration of vasopressor administration, and the timing of antibiotic administration were not routinely recorded; these variables could be considered confounders of AKI risk. Fifth, novel AKI biomarkers were not evaluated prospectively to assess their early predictive utility. Lastly, long-term renal outcomes, including rates of chronic kidney disease progression among AKI survivors, were not assessed because of the brief follow-up period. In particular, norepinephrine was the primary first-line vasopressor used, in line with Surviving Sepsis Campaign guidelines; however, the maximum dose, cumulative dose, and duration of vasopressor support were not recorded, precluding a dose-dependent analysis of AKI risk. Additionally, a standardized resuscitation protocol was not uniformly applied during the 2019–2024 study period, and individual clinical judgment introduced variability in fluid management and vasopressor initiation that may have confounded the association with AKI.

Future research should involve prospective multicenter cohort studies using standardized AKI biomarker measurement protocols as well as structured postoperative surveillance algorithms. Studies evaluating specific interventions such as preoperative nutritional optimization, nephroprotective perioperative fluid protocols, and early goal-directed sepsis management based on real-time AKI biomarkers are also justified. We speculate that the development and external validation of a composite preoperative risk score integrating ASA status, albumin, baseline creatinine, and hernia complexity may further optimize individualized risk communication and resource allocation for patients undergoing LHHR.

CONCLUSION

Postoperative sepsis following LHHR occurs in approximately 1 in 5 patients and carries significant morbidity. AKI is a crucial contributor to in-hospital mortality, occurring in 42.9% of patients with sepsis, and all deaths in our cohort were recorded exclusively in the AKI subgroup. Independent predictors of sepsis were ASA class ≥ III, prolonged operative time, and preoperative hypoalbuminemia. Independent predictors of AKI among patients with sepsis were SOFA score ≥ 8, vasopressor requirement at sepsis onset, and elevated preoperative creatinine (OR 3.14, 95%CI: 1.03–9.61, P = 0.044). KDIGO staging combined with SOFA scoring provides superior mortality discrimination compared with either tool alone. The risk of AKI may be mitigated by preoperative nutritional optimization, renal risk assessment, and careful postoperative monitoring for early organ dysfunction. The utility of novel AKI biomarkers combined with structured preventive interventions requires confirmation in prospective multicenter trials to translate these findings into clinical action for improved outcomes.