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Luo DW, Du HL, Duan WX. Acute kidney injury after liver cancer ablation: Risk factors and perioperative management. World J Gastrointest Surg 2026; 18(11): 124030 [DOI: 10.4240/wjgs.124030]
Author contributions: Luo DW designed the research and wrote the first manuscript; Luo DW, Du HL and Duan WX contributed to conceiving the research and analyzing data; Duan WX conducted the analysis and provided guidance for the research; all authors reviewed and approved the final manuscript.
AI contribution statement: No AI tools were used in this study.
Institutional review board statement: This study was approved by the Ethic Committee of The First Affiliated Hospital of Xi’an Jiaotong University.
Informed consent statement: Informed consent was exempted due to the retrospective design of this study.
Conflict-of-interest statement: There is no conflict of interest.
Data sharing statement: No additional data are available.
Corresponding author: Wan-Xing Duan, Department of Hepatobiliary Surgery, The First Affiliated Hospital of Xi'an Jiaotong University, No. 277 Yanta West Road, Yanta District, Xi’an 710061, Shaanxi Province, China. duanwan3@163.com
Received: July 10, 2026 Revised: August 19, 2026 Accepted: October 9, 2026 Published online: November 27, 2026 Processing time: 124 Days and 18.4 Hours
Abstract
BACKGROUND
Evidence regarding the risk factors for and clinical management of acute kidney injury (AKI) following liver cancer (LC) ablation remains limited.
AIM
To investigate the incidence and potential risk factors for AKI following LC ablation and explore relevant clinical preventive strategies.
METHODS
This retrospective study included 168 patients with LC who underwent ablation between May 2022 and February 2026. Patients were classified into AKI (n = 25) and non-AKI (n = 143) groups according to postoperative AKI occurrence. Baseline characteristics, tumor-related characteristics (laterality, TNM stage, tumor size, tumor number, and ablation type), and laboratory parameters were compared between groups. Univariate and multivariable logistic regression analyses were performed to identify factors associated with AKI after LC ablation.
RESULTS
Age, diabetes, TNM stage, tumor size, hemoglobin (Hb), uric acid (UA), and serum creatinine (SCr) differed significantly between groups. Univariate analysis identified older age, diabetes, larger tumor size, higher UA, and higher SCr levels as potential risk factors, while higher Hb was associated with a lower risk of AKI. Multivariate analysis identified Hb and SCr as independent factors associated with AKI, with higher Hb associated with a lower risk [odds ratio (OR): 0.908, 95% confidence interval (CI): 0.867-0.950, P < 0.001] and higher SCr associated with an increased risk (OR: 1.040, 95%CI: 1.004-1.078, P = 0.031).
CONCLUSION
Lower preoperative Hb and higher preoperative SCr levels may increase the risk of AKI after LC ablation. Preoperative anemia management and renal function assessment may help identify high-risk patients and guide individualized perioperative renal protection strategies.
Core Tip: This retrospective study evaluated risk factors for acute kidney injury (AKI) after liver cancer (LC) ablation in 168 patients (AKI group, n = 25; non-AKI group, n = 143). Low preoperative hemoglobin and high creatinine levels were independently associated with increased AKI risk after LC ablation. Preoperative anemia management and careful renal function monitoring may help identify high-risk patients and guide perioperative renal protection.
Citation: Luo DW, Du HL, Duan WX. Acute kidney injury after liver cancer ablation: Risk factors and perioperative management. World J Gastrointest Surg 2026; 18(11): 124030
Liver cancer (LC) ranks sixth among the most prevalent cancers worldwide and is the third leading cause of cancer-related mortality[1]. Several factors, including viral infection, tobacco use, alcohol consumption, aflatoxin exposure, metabolic syndrome, and obesity, increase the risk of LC[2]. Globally, LC accounts for approximately 830000 deaths and 910000 new cases annually, with Asia accounting for 72% of the global incidence[3]. LC ablation is a local treatment modality that includes radiofrequency ablation (RFA), microwave ablation (MVA), and cryoablation. It is indicated for patients with early-stage LC who have well-preserved liver function (Child-Pugh class A/B), no vascular invasion or extrahepatic metastasis, and tumors measuring ≤ 5 cm in diameter for unifocal disease or ≤ 3 cm for multifocal disease (≤ 3 tumors)[4-6]. A meta-analysis showed that, for solitary hepatocellular carcinoma (HCC) ≤ 3 cm in diameter, ablation and surgical resection provide comparable overall survival outcomes[7]. In some patients with intermediate- or advanced-stage LC, ablation may be used as a palliative therapy or as part of a downstaging strategy in combination with transarterial chemoembolization (TACE), particularly when other treatments are contraindicated or poorly tolerated[8,9]. However, LC ablation may cause erythrocyte destruction, resulting in the release of cell-free hemoglobin (Hb) into the circulation and its subsequent filtration by the glomeruli. The ensuing intravascular hemolysis and hemoglobinuria can cause renal tubular injury, potentially leading to postoperative acute kidney injury (AKI)[10]. AKI is a serious acute complication characterized by a rapid decline in renal function over hours to days. It can promote the development of chronic kidney disease and increase healthcare burden and mortality[11,12]. Older age, comorbidities, and greater exposure to nephrotoxic medications have been identified as risk factors for AKI. Therefore, determining the underlying etiology of AKI is crucial for timely and targeted treatment[13].
Currently, evidence regarding the risk factors for and clinical management of AKI following LC ablation remains limited. Therefore, this study aimed to identify the risk factors for post-ablation AKI and develop corresponding intervention strategies.
MATERIALS AND METHODS
Patient data
This retrospective study included 168 patients who underwent LC ablation at the First Affiliated Hospital of Xi’an Jiaotong University between May 2022 and February 2026. Based on the occurrence of AKI (yes/no), patients were assigned to the AKI group (n = 25) or the non-AKI group (n = 143). AKI was diagnosed when serum creatinine (SCr) increased by ≥ 0.3 mg/dL (26.5 μmol/L) within 48 hours after surgery or to ≥ 1.5 times the preoperative level within 7 days postoperatively. Patients were screened according to the following eligibility and exclusion criteria.
Eligibility criteria: (1) Meeting the diagnostic criteria for HCC[14]; (2) Aged 18-80 years; (3) Undergoing initial treatment and meeting the indications for LC ablation; (4) Having Child-Pugh class A or B liver function[15]; (5) Having an Eastern Cooperative Oncology Group performance status of 0-1[16]; (6) Having undergone preoperative contrast-enhanced computed tomography (CT) or magnetic resonance imaging (MRI) within 1 month before ablation; (7) Having no portal vein tumor thrombus; (8) Having no severe portal hypertension; (9) Having no cognitive or communication impairment; and (10) Having complete clinical data.
Exclusion criteria: (1) Preoperative AKI; (2) AKI attributable to other causes, such as liver/heart/respiratory failure or sepsis; (3) Extrahepatic metastasis or vascular invasion; (4) Other malignant tumors; (5) A history of liver surgery, except TACE or other downstaging treatment; (6) A history of systemic antitumor therapy, including targeted therapy or immunotherapy; (7) Refractory ascites or moderate-to-large volume ascites requiring paracentesis and drainage; (8) Tumors adjacent to critical structures, including the gallbladder, colon, duodenum, diaphragm, or heart, that could not be adequately separated using protective measures such as artificial ascites or artificial pleural effusion; (9) Allergy to MRI or CT contrast agents; (10) Hepatofugal portal venous flow or hepatic arterioportal shunts; (11) Myocardial infarction or unstable angina within the preceding 6 months; (12) Coagulation, cardiac, or pulmonary dysfunction; (13) Allergy to medications or anesthetic agents required for ablation; (14) Active infection or serious uncontrolled diabetes, hypertension, acquired immunodeficiency syndrome, or other systemic diseases; and (15) Pregnancy or lactation.
The etiology of postoperative AKI was determined according to previously reported criteria[17]. Infection-related AKI was defined as AKI occurring in the presence of an identifiable site of infection accompanied by systemic inflammatory response syndrome or sepsis-related manifestations. Drug-induced AKI was defined as AKI occurring after exposure to drugs with established nephrotoxic potential, including aminoglycosides, vancomycin, and contrast agents, within the 3 days preceding AKI onset. Shock-associated AKI was defined as AKI occurring in the presence of systolic blood pressure < 90 mmHg for > 30 minutes or requiring vasoactive agents to maintain blood pressure. Patients meeting any of these criteria were excluded from the study.
Methods
Ablation was performed by percutaneous puncture under ultrasound or CT guidance. RFA or MVA was selected based on lesion size, location, and its relationship with adjacent organs. For MWA, a 2450-MHz water-cooled microwave antenna system (Cool-tip system) was used, with a power output of 60-80 W and a single ablation time of ≤ 10 minutes. RFA was performed using a water-cooled bipolar system with a power output of 30-40 W, and the ablation time was set according to tumor size and electrode-tip length. The ablation zone extended at least 0.5-1.0 cm beyond the tumor margin to ensure an adequate safety margin. The trajectory and puncture path of the ablation needle were planned to avoid large blood vessels and bile ducts.
Postoperative management
Routine support: Patients resumed a normal diet after a 2-4-hour fasting period and remained on bed rest for 6 hours. Renal function monitoring included SCr, blood urea nitrogen (BUN), and urinalysis, with particular attention to occult blood and hemoglobinuria. These parameters were assessed within 24 hours before surgery and on postoperative days 1, 3, and 7 (or before discharge).
Hydration protocol: During and after surgery, patients received continuous intravenous infusion of 0.9% sodium chloride at a rate of 1.0-1.5 mL/kg/hour until 24 hours after the operation. For patients with heart failure or underlying renal insufficiency, the infusion rate was adjusted to 0.5-1.0 mL/kg/hour. The target urine volume was ≥ 0.5 mL/kg/hour.
Urine alkalization protocol: Patients with gross or microscopic hemoglobinuria received intravenous sodium bicarbonate, initially at 1 mmol/kg followed by 0.5 mmol/kg/hour, to maintain a urine pH of 7.0-8.0 for 6-12 hours.
Management of oliguria and AKI: Patients with oliguria (< 0.5 mL/kg/h for > 6 hours) who responded poorly to hydration received furosemide (20-40 mg intravenously as a bolus), as clinically appropriate. Patients with stage 3 AKI or indications for renal replacement therapy (severe hyperkalemia, metabolic acidosis, or pulmonary edema) were transferred to the nephrology department or intensive care unit (ICU) for further management. All procedures and perioperative management were conducted in accordance with standardized protocols and pathways. All ablation procedures were performed by attending physicians or senior physicians with over 5 years of clinical experience in interventional ultrasound or hepatobiliary surgery.
The following patient data were collected from the hospital’s electronic medical record system: Baseline characteristics [sex, age, body mass index (BMI), hypertension, diabetes, hyperlipidemia, smoking and alcohol consumption history]; pathological and tumor-related characteristics (tumor location, maximum tumor diameter, tumor number, TNM stage, and ablation type); and laboratory parameters [Hb, total bilirubin (TBIL), serum albumin (ALB), BUN, uric acid (UA), SCr, serum sodium, high-/Low-density lipoprotein cholesterol (HDL-C)/(LDL-C)].
Data processing and statistical methods
SPSS 26.0 (IBM Corp., Armonk, NY, United States) was employed for data analysis. Continuous variables were expressed as mean ± SD and compared between groups using the t-test. Categorical variables were presented as n (%) and compared using the χ2 test. Univariate and multivariate analyses were performed using binary logistic regression. Variables with P < 0.10 in the univariate analysis were entered into the multivariable logistic regression model using the enter method. P values < 0.05 were considered statistically significant.
RESULTS
Baseline characteristics
The incidence of AKI after LC ablation was 14.88% among the 168 patients. The AKI and non-AKI groups were comparable in terms of sex, BMI, hypertension, hyperlipidemia, and smoking and alcohol consumption history (all P > 0.05). Patients who developed AKI were older than those who did not (61.68 ± 8.91 years vs 56.62 ± 10.33 years, P < 0.05) and had a higher prevalence of diabetes (44.00% vs 21.68%, P < 0.05; Table 1).
The two groups were comparable with respect to tumor location, tumor number, and ablation type (all P > 0.05). TNM stage and tumor size were significantly associated with AKI (P < 0.05). Compared with the non-AKI group, the AKI group had a higher proportion of patients with TNM stage III–IV disease (32.00% vs 15.38%) and a larger mean tumor size (4.96 ± 2.40 cm vs 3.98 ± 1.48 cm, P < 0.05; Table 2).
Hb levels were lower in patients with AKI than in those without AKI (114.20 g/L ± 16.53 vs 135.46 ± 13.79 g/L, P < 0.05), while UA (383.36 ± 110.99 μmol/L vs 341.54 ± 82.64 μmol/L, P < 0.05) and SCr (93.08 ± 24.15 μmol/L vs 77.73 ± 16.59 μmol/L, P < 0.05) levels were higher. No significant between-group differences were observed regarding TBIL, serum ALB, BUN, serum sodium, HDL-C, and LDL-C (all P > 0.05; Table 3).
Age, diabetes, TNM stage, tumor size, Hb, UA, and SCr, which showed significant between-group differences in the preceding analyses, were included as independent variables, while postoperative AKI was treated as the dependent variable. Variables were appropriately coded for regression analysis (Table 4).
Univariate binary logistic regression analysis showed that age ≥ 60 years [odds ratio (OR) = 2.762, P = 0.024], diabetes (OR = 2.839, P = 0.021), tumor size (OR = 1.386, P = 0.009), UA (OR = 1.005, P = 0.032), and SCr (OR = 1.045, P < 0.001) were associated with an increased risk of AKI after LC ablation. Higher Hb levels were associated with a lower risk of AKI (OR = 0.900, P < 0.001). TNM stage was not significantly associated with AKI (P = 0.051; Table 5).
Table 5 Univariate analysis of acute kidney injury after hepatocellular carcinoma ablation.
Multivariate logistic regression analysis showed that higher Hb levels were independently associated with a lower risk of postoperative AKI [OR = 0.908, 95% confidence interval (CI): 0.867-0.950, P < 0.001]. Specifically, each 1 g/L increase in preoperative Hb was associated with an approximately 9.2% reduction in the odds of postoperative AKI. Higher preoperative SCr levels were independently associated with elevated postoperative AKI risk (OR = 1.040, 95%CI: 1.004-1.078, P = 0.031), with each 1 μmol/L increase in preoperative SCr increasing AKI risk by 4.0%. Age, diabetes, TNM stage, tumor size, and UA were not independently associated with AKI after LC ablation (P > 0.05; Table 6).
Table 6 Multivariate analysis of acute kidney injury after liver cancer ablation.
AKI is a common and serious complication among hospitalized patients and is characterized by an abrupt decline in glomerular filtration rate. Its diagnosis is primarily based on decreased urine volume and increased SCr[18]. Pathologically, AKI involves inflammation, endothelial dysfunction, hemodynamic disturbances, and renal tubular injury, all of which are closely related to adverse in-hospital outcomes[19,20]. In the present study, the incidence of AKI following LC ablation was approximately 15% (25/168). Previous studies have reported an AKI incidence of approximately 10%-15% among hospitalized patients, with rates increasing to 50% among patients admitted to the ICU[13]. In addition, the incidence of post-MVA AKI in patients with large liver tumors (≥ 5 cm) has been reported to approach 24%[21]. Thus, the AKI incidence observed in the present study falls within the range reported in previous studies.
Analysis of baseline characteristics, tumor-related parameters, and laboratory findings showed that age, diabetes, TNM stage, tumor size, Hb, UA, and SCr were associated with AKI post-LC ablation. Univariate logistic regression analysis further indicated that older age, diabetes, larger tumor size, and higher UA and SCr levels were associated with an increased risk of post-ablation AKI, whereas higher Hb levels appeared to be protective.
Multivariable analysis further confirmed that Hb was independently associated with a lower risk of AKI after LC ablation, while SCr independently increased the risk. An age > 60 years generally reflects an age-related physiological decline in renal functional reserve[22]; however, its independent association with AKI may have been attenuated after adjustment for SCr. Diabetes may also increase susceptibility to AKI, potentially through endothelial dysfunction, which can increase renal vascular responsiveness to vasoconstriction, impair renal perfusion, and contribute to glomerular hyperfiltration[23]. Such chronic renal injury may be clinically reflected by elevated preoperative SCr levels. In the present multivariable analysis, the association between diabetes and AKI was attenuated after adjustment for SCr and was no longer statistically significant, suggesting that baseline renal function may partly account for this association.
Larger tumor size may require a longer ablation time and consequently result in greater erythrocyte destruction[24]. However, the association between tumor size and AKI may be partly mediated by Hb levels, attenuating its independent effect after multivariable adjustment. Elevated UA levels may contribute to renal injury through oxidative stress[25]. However, UA was no longer significantly associated with AKI after adjustment for SCr, suggesting that its predictive value may be partly attributable to underlying renal function. Hb was identified as an independent protective factor against AKI after LC ablation. This may be related to Hb’s role in maintaining renal oxygen delivery, particularly in the metabolically active outer medulla, which is highly susceptible to hypoxia. Anemia can reduce oxygen delivery and increase the risk of renal hypoxic injury[26]. In a study by Graw et al[27], increased plasma levels of circulating cell-free hemoglobin (CFH) in patients with severe ARDS treated with venovenous extracorporeal membrane oxygenation were independently associated with AKI, and higher plasma haptoglobin concentrations appeared to mitigate CFH-associated AKI. These findings are consistent with the proposed role of hemolysis and free Hb in AKI and suggest that strategies targeting free Hb, such as haptoglobin supplementation, may warrant further investigation for the prevention of post-ablation AKI. Preoperative SCr reflects baseline renal function, and by extension, renal functional reserve. Its independent association with AKI after LC ablation may reflect a reduced renal capacity to compensate for ablation-induced hemolytic injury in patients with impaired baseline renal function[28]. Yang et al[29] reported that preoperative SCr ≥ 110 μmol/L and an MVA duration ≥ 20 minutes were independent risk factors for AKI after MVA for LC, which is consistent with the present findings. Collectively, these findings support a potential pathophysiological framework linking anemia, hemolysis, and baseline renal function. Preoperative low Hb may reduce oxygen delivery and thereby diminish renal oxygen reserve[30]. During ablation, erythrocyte hemolysis may release cell-free Hb, which is filtered and metabolized in the kidneys. Excess free Hb and its heme-derived products can promote oxidative stress and endoplasmic reticulum stress, resulting in direct tubular epithelial injury[31]. When baseline renal functional reserve is reduced, the kidneys may have a limited capacity to compensate for this additional injury, ultimately resulting in a significant increase in SCr[32,33].
The novelty of this study lies in identifying Hb, in addition to confirming preoperative SCr, as an independent factor associated with AKI after LC ablation. These findings may provide a basis for perioperative risk stratification and targeted prevention of post-ablation AKI in patients with LC, with potential implications for clinical practice.
Based on the present findings and supporting evidence from previous studies, we propose that targeted strategies for preventing AKI after LC ablation should focus on the following aspects. First, accurately evaluating preoperative renal function is critical. Routine measurement of SCr is recommended to identify high-risk patients[29]. Second, anemia should be actively corrected before the operation. In selected patients, Hb levels should be optimized through iron supplementation, erythropoietin, or blood transfusion, as appropriate, to improve renal oxygen delivery and potentially increase the kidney’s tolerance to hemolysis-related injury, particularly in patients with iron-deficiency anemia[21]. Iron-deficiency anemia has been reported to be an independent predictor of AKI after hepatectomy. Iron supplementation may alleviate iron-mediated oxidative stress and reduce susceptibility to nephrotoxic AKI, suggesting that patients with iron deficiency may derive particular benefit from iron replacement[34,35]. In addition, tumor-related anemia is common in patients with HCC (reported prevalence 44%) and has been independently associated with mortality. Such anemia is often related to chronic inflammation, and management should therefore address the underlying inflammatory state and impaired iron utilization[36]. Accordingly, individualized treatment strategies based on the underlying cause of anemia may help reduce the risk of postoperative AKI. Third, when clinically feasible, the duration of ablation should be minimized, with an ablation time of < 20 minutes suggested as a potential target[29]. Fourth, adequate perioperative hydration and urinary alkalization, when clinically indicated, with close postoperative monitoring of urine color/volume and SCr may facilitate early identification and prompt intervention[37]. Importantly, the effectiveness of the proposed preventive strategies requires further validation in prospective clinical studies.
This study has several limitations. First, the sample comprised 168 patients who underwent LC ablation at a single center in one region, which may limit the generalizability of the findings. Future studies involving larger cohorts from multiple regions and institutions are warranted to improve the representativeness of the study population. Second, potentially relevant procedural factors, including cumulative ablation energy, ablation volume, and ablation duration, as well as the severity and duration of postoperative hemoglobinuria, were not collected. Prospective studies should incorporate these parameters to better quantify their independent associations with AKI risk. Third, the retrospective single-center design and the 4-year study period may have introduced confounding. Although a consistent perioperative management protocol was used at our center, changes in ablation equipment and the learning curve associated with increasing operator experience may have influenced treatment outcomes. Multi-center prospective studies are therefore needed to validate these findings. Fourth, this study did not determine optimal Hb cut-off values for predicting AKI risk. Future studies should use stratified analyses and receiver operating characteristic curve analysis to identify clinically meaningful Hb thresholds and further assess their predictive value. Finally, because of the study design and available data, we did not evaluate AKI severity according to KDIGO staging, length of hospital stay, requirement for renal replacement therapy, readmission, or long-term renal function outcomes. Future prospective studies incorporating multidimensional clinical outcomes and long-term follow-up are warranted to provide a more comprehensive assessment of AKI after LC ablation and to facilitate clinically useful risk stratification.
CONCLUSION
Preoperative low Hb and elevated SCr levels were independently associated with an increased risk of AKI after LC ablation. These findings highlight the importance of preoperative assessment and appropriate management of anemia, as well as accurate evaluation of baseline renal function. Individualized perioperative renal protection strategies based on these risk factors may help reduce the risk of post-ablation AKI.
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