A low preoperative platelet-to-white blood cell ratio is associated with acute kidney injury following cerebral aneurysm treatment in South Korea

Seung-Woon Lim; Woo-Young Jo; Hee-Pyoung Park

doi:10.4266/acc.003120

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Original Article Neurosurgery A low preoperative platelet-to-white blood cell ratio is associated with acute kidney injury following cerebral aneurysm treatment in South Korea: Seung-Woon Lim¹, Woo-Young Jo², Hee-Pyoung Park²; Acute and Critical Care 2025;40(1):59-68.
DOI: https://doi.org/10.4266/acc.003120
Published online: February 21, 2025

¹Department of Anesthesiology and Pain Medicine, Chung-Ang University Hospital, Seoul, Korea

²Department of Anesthesiology and Pain Medicine, Seoul National University Hospital, Seoul National University College of Medicine, Seoul, Korea

Corresponding author: Hee-Pyoung Park Department of Anesthesiology and Pain Medicine, Seoul National University Hospital, Seoul National University College of Medicine, 101 Daehak-ro, Jongno-gu, Seoul 03080, Korea Tel: +82-2-2072-2466, Fax: +82-2-747-5639, E-mail: hppark@snu.ac.kr

• Received: August 1, 2024 • Revised: November 30, 2024 • Accepted: December 3, 2024

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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Abstract
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
KEY MESSAGES
NOTES
SUPPLEMENTARY MATERIALS
REFERENCES

Abstract

Background
Inflammation is involved in the pathophysiology of postoperative acute kidney injury (AKI). We investigated whether preoperative platelet-to-white blood cell ratio (PWR), a novel serum biomarker of systemic inflammation, was associated with postoperative AKI following cerebral aneurysm treatment. We also compared the discrimination power of preoperative PWR with those of other preoperative systemic inflammatory indices in predicting postoperative AKI.
Methods
Perioperative data including preoperative systemic inflammatory indices and cerebral aneurysm-related variables were retrospectively analyzed in 4,429 cerebral aneurysm patients undergoing surgical clipping or endovascular coiling. Based on the cutoff value of preoperative PWR, patients were divided into the high PWR (≥39.04, n=1,924) and low PWR (<39.04, n=2,505) groups. After propensity score matching (PSM), 1,168 patients in each group were included in the data analysis. AKI was defined according to the Kidney Disease Improving Global Outcomes guidelines.
Results
Postoperative AKI occurred more frequently in the low PWR group than in the high PWR group before PSM (45 [1.8%] vs. 7 [0.4%], P<0.001) and after (17 [1.5%] vs. 5 [0.4%], P=0.016). A low preoperative PWR was predictive of postoperative AKI before PSM (odds ratio [95% CI], 3.93 [1.74–8.87]; P<0.001) and after (3.44 [1.26–9.34], P=0.016). Preoperative PWR showed the highest area under the curve for postoperative AKI (0.713 [0.644–0.782], P<0.001), followed by preoperative platelet-to-neutrophil ratio (0.694 [0.619–0.769], P<0.001), neutrophil percentage-to-albumin ratio (0.671 [0.592–0.750], P<0.001), white blood cell-to-hemoglobin ratio (0.665 [0.579–0.750], P<0.001), neutrophil-to-lymphocyte ratio (0.648 [0.569–0.728], P<0.001), and systemic inflammatory index (0.615 [0.532–0.698], P=0.004).
Conclusions
A low preoperative PWR was associated with postoperative AKI following cerebral aneurysm treatment.
Key Words: acute kidney injury; cerebral aneurysm; platelet; white blood cell

INTRODUCTION

Cerebral aneurysms are typically treated through surgical clipping or endovascular coiling. Postoperative acute kidney injury (AKI) can arise as a complication following these treatments. This condition is strongly associated with increased long-term mortality and poor short-term neurological outcomes in patients with aneurysmal subarachnoid hemorrhage [1-3]. Therefore, identifying risk factors for postoperative AKI after cerebral aneurysm treatment is clinically important. Early identification of high-risk patients facilitates effective redistribution of hospital resources. Unfortunately, few clinical studies have investigated the risk factors for postoperative AKI in patients undergoing cerebral aneurysm treatment. Previous studies have identified several independent predictors for developing postoperative AKI, including preoperative hypoalbuminemia, aneurysmal subarachnoid hemorrhage, male sex, phenylephrine use, low preoperative hemoglobin level, low estimated glomerular filtration rate, large aneurysm, and premorbid hypertension [2,4,5]. Additional studies are needed to further identify these risk factors in patients undergoing cerebral aneurysm treatment.

Inflammation plays a crucial role in the pathophysiological mechanisms of AKI development and significantly impacts the clinical course and associated morbidity of AKI [6-8]. Various systemic inflammatory indices, including the neutrophil percentage-to-albumin ratio (NPAR), neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), white blood cell-to-hemoglobin ratio (WHR), prognostic nutritional index (PNI), and systemic immune-inflammation index (SII), are independent risk factors for AKI [9-15]. The platelet-to-white blood cell ratio (PWR) is a novel serum biomarker of systemic inflammation. A low PWR is strongly associated with poor prognosis in several conditions, including acute ischemic stroke, acute-on-chronic liver failure, nephrectomy for renal malignancy, and aneurysmal subarachnoid hemorrhage [16-20]. However, no clinical investigations have examined the relationship between preoperative PWR and postoperative AKI in patients undergoing cerebral aneurysm treatment.

In this study, we tested the hypothesis that preoperative PWR is associated with postoperative AKI following cerebral aneurysm treatment. We also compared the discrimination power of preoperative PWR with other preoperative systemic inflammatory indices in predicting postoperative AKI.

MATERIALS AND METHODS

This retrospective study was approved by the Institutional Review Board at Seoul National University Hospital (No. H-2407-120-1554), with a waiver of the requirement for written informed consent. The study adhered to the principles of the Declaration of Helsinki.

Subjects

Patients who underwent endovascular coiling or surgical clipping for cerebral aneurysm securement at Seoul National University Hospital between January 2006 and December 2019 were included. Exclusion criteria were preoperative chronic renal disease, external ventricular drainage catheter insertion without securing the aneurysm, pseudoaneurysm, documented preoperative infection, and missing data on preoperative platelet and white blood cell (WBC) counts. In addition, patients with missing data on serum albumin level and WBC differential counts were excluded, as low preoperative albumin levels and high preoperative NLR are strongly associated with postoperative AKI in neurosurgical patients and those undergoing various surgical procedures [4,9,14,21,22].

Data Collection

Two anesthesiologists retrospectively reviewed the patients’ electronic medical records to obtain the following information: demographics (age, sex, and body mass index), comorbidities (hypertension, diabetes mellitus, pulmonary disease, cardiac disease, and hepatic disease), cerebral aneurysm-related variables (location, number, largest diameter, rupture status, and recanalization), preoperative laboratory data within at least 1 month before treatment (hemoglobin and albumin levels, platelet, WBC, neutrophil, and lymphocyte counts), preoperative systemic inflammatory indices (PWR, NPAR, NLR, platelet-to-neutrophil ratio [PNR], PLR, WHR, PNI, and SII), intraoperative variables (emergency status, operation type, anesthetic time, total time and area of mean blood pressure [MBP] <65 mm Hg, time-weighted average of MBP <65 mm Hg, fluid balance, transfusion, and maximum lactate level), and clinical course (intensive care unit [ICU] admission, ICU and hospital lengths of stay, and in-hospital mortality).

Postoperative AKI

Postoperative AKI was diagnosed and staged based on the Kidney Disease Improving Global Outcomes clinical practice guidelines for AKI, which utilize changes in serum levels of creatinine to stratify patients into three stages of AKI severity [23]. In stage 1, creatinine levels increase by ≥0.3 mg/dl from preoperative baseline within 48 hours postoperatively or becomes 1.5–1.9 times higher than the preoperative baseline within 7 days postoperatively. In stage 2, they are 2.0–2.9 times higher than the preoperative baseline. In stage 3, they are ≥4.0 mg/dl from the preoperative baseline and become three times higher than the preoperative baseline, or renal replacement therapy is required.

Systemic Inflammatory Indices

The formulas used to calculate preoperative systemic inflammatory indices were as follows:

PWR=platelet count (×10⁹/L)/WBC count (×10⁹/L)

NPAR=neutrophil percentage×100/serum albumin level (g/dl)

NLR=neutrophil count (×10⁹/L)/lymphocyte count (×10⁹/L)

PNR=platelet count (×10⁹/L)/neutrophil count (×10⁹/L)

PLR=platelet count (×10⁹/L)/lymphocyte count (×10⁹/L)

WHR=WBC count (×10⁹/L)/hemoglobin level (g/dl)

PNI=10×serum albumin level (g/dl)+5×lymphocyte count (×10⁹/L)

SII=platelet count (×10⁹/L)×neutrophil count (×10⁹/L)/lymphocyte count (×10⁹/L)

Outcomes

The primary outcome was the association between preoperative PWR and postoperative AKI. The secondary outcome was the discrimination ability of various preoperative systemic inflammatory indices for postoperative AKI.

Sample Size Calculation and Statistical Analysis

Based on a previous study, which reported a 1.9% incidence of postoperative AKI after surgical clipping for cerebral aneurysm [4], we assumed no significant difference in the incidence between surgical clipping and endovascular coiling. Therefore, a sample size of at least 4,102 patients was required to reproduce this incidence with a 99% CI and a 0.55% margin of error.

Statistical analyses were conducted using IBM SPSS Statistics 26 (IBM Corp.) and MedCalc Statistical Software version 22.0. Missing data were replaced using the median imputation method. Categorical variables, continuous variables with normal distribution, and continuous variables with skewed distribution were presented as numbers (percentages), means±standard deviation, and medians with interquartile range, respectively. Categorical variables were compared using the chi-square test or Fisher’s exact test. Continuous variables with normal and skewed distributions were compared using Student t-test and Mann-Whitney U-test, respectively.

The area under the curve (AUC) for preoperative systemic inflammatory indices for discriminating postoperative AKI was calculated using receiver operating characteristic (ROC) analysis. The DeLong test was used to compare AUCs between preoperative PWR and other preoperative systemic inflammatory indices. The optimal cutoff value was defined as the value that maximized the sum of sensitivity and specificity for postoperative AKI.

Patients were divided into two groups based on the optimal cutoff value of preoperative PWR: high and low PWR groups. propensity score matching (PSM) was performed between the two groups to control for confounding effects of other preoperative variables on postoperative AKI. Demographics (age, sex, and body mass index), aneurysm-related variables (location, number, largest diameter, and rupture status), emergency operation, operation type, and preoperative laboratory variables (hemoglobin and albumin levels, lymphocyte, and neutrophil counts) were included in PSM.

Before PSM, variables with a P-value <0.05 in univariate regression analysis, except for intraoperative maximum lactate level (due to small sample size), were included in multivariate regression analysis to identify independent predictors of postoperative AKI. After PSM, univariate regression analysis was performed to determine the association between preoperative PWR and postoperative AKI. For subgroup analysis, patients were divided into endovascular coiling and surgical clipping groups. Multivariate regression analysis was conducted to identify the variables associated with postoperative AKI in each treatment group. A P-value <0.05 was considered statistically significant.

RESULTS

A total of 4,802 patients presented during the study period. Of these, 373 patients were excluded for the following reasons: preoperative chronic kidney disease (n=95), lack of preoperative laboratory data (n=270), untreated aneurysm (n=4), preoperative infection (n=3), and pseudoaneurysm (n=1) (Figure 1). Thus, 4,429 patients were finally included. Missing data on intraoperative MBP-related variables were imputed for 26 patients. Postoperative AKI occurred in 52 patients (1.2), including 48 patients with stage 1, three with stage 2, and one with stage 3 AKI. No patient received hemodialysis due to postoperative AKI.

In ROC curve analysis, the optimal cutoff value of preoperative PWR for discriminating postoperative AKI was 39.04. Patients were divided into two groups: high PWR (≥39.04, n=1,924) and low PWR (<39.04, n=2,505). The incidence of postoperative AKI was higher in the low PWR group than in the high PWR group before PSM (1.8% vs. 0.4%, P<0.001) (Table 1). Even after preoperative variables were well matched with a caliper of 0.07 (P=0.842), the incidence of postoperative AKI remained higher in the low PWR group (1.5% vs. 0.4%, P=0.016).

In multivariate regression analysis before PSM, significant associations with postoperative AKI included preoperative serum levels of albumin (odds ratio [95% CI], 0.47 [0.23–0.95]; P=0.035), neutrophil count (1.38 [1.13–1.69], P=0.002), low preoperative PWR (3.93 [1.74–8.87], P<0.001), and intraoperative transfusion (3.27 [1.47–7.31], P=0.004) (Table 2). Low preoperative PWR (3.44 [1.26–9.34], P=0.016) remained significantly associated with postoperative AKI in the univariate regression analysis even after PSM.

In ROC curve analysis, preoperative PWR demonstrated the highest AUC for postoperative AKI (0.713 [0.644–0.782], P<0.001), followed by preoperative PNR (0.694 [0.619–0.769], P<0.001), NPAR (0.671 [0.592–0.750], P<0.001), WHR (0.665 [0.579–0.750], P<0.001), NLR (0.648 [0.569–0.728], P<0.001), and SII (0.615 [0.532–0.698], P=0.004) (Table 3). Preoperative PWR had a higher AUC than preoperative PLR and PNI (0.713 vs. 0.506 and 0.571, P<0.001 and P=0.016, respectively).

In subgroup analysis, postoperative AKI occurred in 38 (1.2) of the 3,213 patients undergoing endovascular coiling and in 14 (1.2) of the 1,246 patients undergoing surgical clipping (Supplementary Table 1). Low preoperative PWR was a common predictor of postoperative AKI regardless of the treatment technique (endovascular coiling: 3.35 [1.26–8.93], P=0.016; surgical clipping: 10.04 [1.30–77.40], P=0.027) (Supplementary Table 2). Aneurysmal rupture (2.54 [1.09–5.90], P=0.030), neutrophil count (1.52 [1.14–2.03], P=0.005), and contrast-induced AKI (233.32 [82.75-657.90], P<0.001) were predictive of postoperative AKI in patients undergoing endovascular coiling, while intraoperative transfusion (8.22 [2.80–24.19], P<0.001) was a predictor among those undergoing surgical clipping. Among 3,213 patients undergoing endovascular coiling, contrast-induced AKI, which is defined as a 25% increase in serum creatinine or a 0.5 mg/dl increase in absolute serum creatinine within 72 hours of the contrast injection [24], was shown in 137 patients (4.3%). Preoperative PWR was 36.1±14.7 and 37.9±13.2 in patients with contrast-induced AKI and those without (P=0.103) (Supplementary Table 3). Regarding clinical outcomes, patients with postoperative AKI had a longer ICU stay and a higher in-hospital mortality rate compared to those without postoperative AKI (Table 4).

DISCUSSION

This study was the first to investigate the association between preoperative PWR and postoperative AKI following cerebral aneurysm treatment. Our results indicated that preoperative PWR was a significant independent predictor of postoperative AKI with acceptable discrimination ability. A low preoperative PWR was associated with postoperative AKI, with an odds ratio of 3.4 in patients undergoing cerebral aneurysm treatment. In addition, preoperative neutrophil count emerged as a significant predictor of postoperative AKI in multivariate logistic analysis before PSM. These findings suggested that leukocytes, particularly neutrophils, are closely related to the development of postoperative AKI, which can be partially explained by the cellular and molecular mechanisms of inflammation in response to kidney injury [25,26]. Acute injurious stimuli, such as inflammation, sepsis, and ischemia, are detected by renal dendritic cells and macrophages, resulting in the secretion of cytokines and chemokines. Consequently, leukocytes, particularly neutrophils, migrate from blood vessels to the injury site and release toxic granule contents to destroy invading pathogens. However, this non-specific reaction can also induce renal tissue damage. Consistent with our findings, several previous studies have demonstrated that serum biomarkers reflecting systemic inflammation, including NPAR, NLR, PLR, WHR, PNI, and SII, are significant independent predictors of AKI in various patient populations [9-15]. Altogether, these findings support the notion that systemic inflammation is a major pathophysiological factor for AKI.

The present study investigated the best preoperative inflammatory index for discriminating postoperative AKI. The highest AUC for postoperative AKI was observed for preoperative PWR, followed by preoperative PNR, NPAR, WHR, NLR, and SII (Table 3). Notably, only preoperative PWR demonstrated good discrimination ability for postoperative AKI, while the remaining preoperative inflammatory indices showed fair discrimination ability. Although the difference in AUC between preoperative PWR and other preoperative inflammatory indices (PNR, NPAR, WHR, NLR, and SII) was not statistically significant, the AUC for preoperative PWR was significantly higher than those for preoperative PLR and PNI. Preoperative PLR and PNI showed poor discrimination ability for postoperative AKI, with AUCs of 0.5–0.6. This suggested that neutrophil- or leukocyte-based inflammatory indices may better predict postoperative AKI than lymphocyte-based inflammatory indices.

Our study also demonstrated a significant negative association between serum albumin level and postoperative AKI, with an odds ratio of 0.47. Similarly, previous studies have shown that preoperative hypoalbuminemia is a risk factor for postoperative AKI in patients undergoing cerebral aneurysmal clipping and brain tumor surgery [4,21]. Albumin has renoprotective properties, improving renal perfusion and glomerular filtration by provoking renal vasodilation and inhibiting apoptosis in renal tubular cells by scavenging reactive oxygen species [27,28]. In addition, intraoperative transfusion was a significant predictor of postoperative AKI, particularly in patients undergoing surgical clipping. Intraoperative massive bleeding and hypotension can reduce perfusion and oxygen delivery to the kidney, resulting in postoperative AKI. In subgroup analysis, aneurysmal subarachnoid hemorrhage was predictive of postoperative AKI in patients undergoing endovascular coiling. Similarly, a previous study demonstrated a significant association between aneurysmal subarachnoid hemorrhage and postoperative AKI in patients undergoing surgical clipping [4]. AKI is a major complication following aneurysmal subarachnoid hemorrhage [2]. Aneurysmal subarachnoid hemorrhage can cause secondary non-neurological multi-organ dysfunction, involving stress-induced cardiomyopathy and neurogenic pulmonary edema, which are commonly accompanied by circulatory shock, resulting in reduced effective circulating blood volume and impaired renal blood flow [29]. Contrast is the most important factor for AKI after coil embolization. In this study, contrast-induced AKI was shown in a total of 137 patients (4.3%) after coil embolization (34 [7.3%] for ruptured cerebral aneurysm and 103 [3.8%] for unruptured cerebral aneurysm) and was significantly associated with postoperative AKI in patients undergoing endovascular treatment. Also, the in-hospital mortality rate was significantly higher in patients with contrast-induced AKI (Supplementary Table 3). Similar to our study, a previous study demonstrated that the incidence of contrast-induced AKI was 7.3% in patients undergoing coil embolization for treatment of aneurysmal subarachnoid hemorrhage and that contrast-induced AKI was strongly associated with poor clinical outcomes of aneurysmal subarachnoid hemorrhage after endovascular treatment [30].

This study had some limitations. First, because of a retrospective study, there remained a possibility of potential biases, including recall and selection biases. Second, the number of patients with postoperative AKI was relatively small. A large-scale multi-center study is needed to validate the relationship between preoperative PWR and postoperative AKI and identify other important risk factors. Third, only preoperative systemic inflammatory indices, including PWR, were used to investigate discrimination ability for postoperative AKI. Previous studies have shown that immediate postoperative systemic inflammatory indices have higher discrimination power than preoperative indices in terms of prognosis in glioblastoma and aneurysmal subarachnoid hemorrhage patients [31,32]. Further research is needed to determine the predictive power of immediate postoperative systemic inflammatory indices for postoperative AKI.

In conclusion, a low preoperative PWR level was significantly associated with postoperative AKI following cerebral aneurysm treatment. Incorporating preoperative PWR level into preoperative evaluation may facilitate the identification of patients at high risk for postoperative AKI.

KEY MESSAGES

▪ Inflammation is involved in the pathophysiology of acute kidney injury (AKI).

▪ Platelet-to-white blood cell ratio (PWR) is a novel serum biomarker of systemic inflammation.

▪ Preoperative PWR was a significant independent predictor of postoperative AKI following cerebral aneurysm treatment with good discrimination ability.

NOTES

CONFLICT OF INTEREST

No potential conflict of interest relevant to this article was reported.

FUNDING

None.

ACKNOWLEDGMENTS

None.

AUTHOR CONTRIBUTIONS

Conceptualization: HPP, SWL. Data collection: HPP, WYJ. Statistical analysis: HPP, WYJ. Writing–original draft: SWL. Writing–review & editing: HPP, WYJ. All authors read and agreed to the published version of the manuscript.

SUPPLEMENTARY MATERIALS

Supplementary materials can be found via https://doi.org/10.4266/acc.003120.

Supplementary Table 1.

Comparisons of demographics, aneurysm-related data, perioperative data and clinical outcomes in patients with postoperative acute kidney injury or without who underwent endovascular coiling or surgical clipping for cerebral aneurysm

acc-003120-Supplementary-Table-1.pdf

Supplementary Table 2.

Univariate and multivariate logistic regression analyses for postoperative acute kidney injury in patients undergoing endovascular coiling or surgical clipping for cerebral aneurysm

acc-003120-Supplementary-Table-2.pdf

Supplementary Table 3.

Comparisons of preoperative platelet-to-white blood cell ratio, postoperative AKI, and in-hospital mortality in patients with contrast-induced acute kidney injury or without who underwent endovascular coiling

acc-003120-Supplementary-Table-3.pdf

Figure 1.

The flowchart of the study. EVD: external ventricular drainage; PWR: platelet-to-white blood cell ratio.

Table 1.

Comparisons of demographics, aneurysm-related data, perioperative data and clinical outcomes in patients with high or low preoperative platelet-to-white blood cell ratio who underwent cerebral aneurysm treatment

Variable	Before matching			After matching
Variable	High PWR (n=1,924)	Low PWR (n=2,505)	P-value	High PWR (n=1,168)	Low PWR (n=1,168)	P-value
Demographics
Age (yr)	59±10	59±11	0.409	59±10	59±10	0.814
Male sex	421 (21.9)	985 (39.3)	<0.001	365 (31.3)	346 (29.6)	0.418
Body mass index (kg/m²)	24.4±3.6	24.6±3.7	0.079	24.5±3.5	24.6±3.8	0.735
Comorbidity
Hypertension	289 (15.0)	373 (14.9)	0.932	194 (16.6)	177 (15.2)	0.365
Diabetes mellitus	45 (2.3)	99 (4.0)	0.003	32 (2.7)	40 (3.4)	0.402
Pulmonary disease	10 (0.5)	18 (0.7)	0.450	4 (0.3)	10 (0.9)	0.178
Cardiac disease	40 (2.1)	60 (2.4)	0.541	24 (2.1)	26 (2.2)	0.886
Hepatic disease	19 (1.0)	29 (1.2)	0.662	13 (1.1)	19 (1.6)	0.373
Aneurysm-related variables
Location			0.133			0.375
Anterior	1,734 (90.1)	2,227 (88.9)		1,067 (91.4)	1,055 (90.3)
Posterior	154 (8.0)	240 (9.6)		82 (7.0)	98 (8.4)
Both	36 (1.9)	38 (1.5)		19 (1.6)	15 (1.3)
Number of aneurysms			0.734			0.908
1	1,639 (85.2)	2,124 (84.8)		995 (85.2)	992 (84.9)
≥2	285 (14.8)	381 (15.2)		173 (14.8)	176 (15.1)
Largest diameter of aneurysm (mm)	5.5±3.5	5.8±3.5	0.009	5.4±3.1	5.6±3.3	0.272
Emergent operation	98 (5.1)	502 (20.0)	<0.001	65 (5.6)	77 (6.6)	0.341
Recanalization	119 (6.2)	154 (6.1)	1.000	71 (6.1)	91 (7.8)	0.122
Coil embolization	1,366 (71.0)	1,847 (73.7)	0.045	840 (71.9)	849 (72.7)	0.711
Ruptured aneurysm	82 (4.3)	506 (20.0)	<0.001	60 (5.1)	62 (5.3)	0.926
Preoperative laboratory findings
Hemoglobin (g/dl)	12.9±1.4	13.4±1.5	<0.001	13.2±1.4	13.1±1.4	0.367
Albumin (g/dl)	4.2±0.3	4.1±0.4	<0.001	4.2±0.3	4.2±0.3	0.313
Platelet count (×10⁹/L)	262.7±59.3	219.9±55.0	<0.001	277.9±58.7	194.6±41.3	<0.001
Lymphocyte count (×10⁹/L)	1.9±0.6	2.2±1.0	<0.001	2.1±0.6	2.1±0.6	0.832
White blood cell count (×10⁹/L)	5.4±1.2	8.1±3.4	<0.001	5.9±1.1	6.0±1.1	0.017
Neutrophil count (×10⁹/L)	0.2±0.1	0.5±0.7	<0.001	0.2±0.1	0.2±0.1	0.053
PWR	49.8±10.8	29.3±7.0	<0.001	47.6±8.6	32.5±4.9	<0.001
Anesthetic time (hr)	2.9±1.4	3.1±1.5	<0.001	2.9±1.4	3.0±1.5	0.088
Intraoperative MBP
Total time of MBP <65 mm Hg (min)	12.0±22.8	16.5±29.5	<0.001	12.8±23.8	15.6±28.0	0.008
Total area of MBP <65 mm Hg (mm Hg×min)	50.4±114.5	72.2±153.1	<0.001	52.4±117.3	64.7±131.0	0.017
TWA of MBP <65 mm Hg (mm Hg)	0.3±0.6	0.4±0.8	<0.001	0.3±0.6	0.4±0.7	0.037
Intraoperative fluid balance (ml/kg/hr)	1.7±2.5	2.1±3.3	<0.001	1.8±2.5	1.9±2.7	0.208
Intraoperative transfusion	64 (3.3)	112 (4.5)	0.064	34 (2.9)	53 (4.5)	0.049
Intraoperative maximum lactate (mmol/L)^a)	1.6±1.2	2.0±1.8	<0.001	1.7±1.2	1.7±1.5	0.574
Acute kidney injury	7 (0.4)	45 (1.8)	<0.001	5 (0.4)	17 (1.5)	0.016
KIDGO stage 1:2:3	6:1:0	42:2:1		4:1:0	17:0:0
ICU admission	664 (34.5)	1,112 (44.4)	<0.001	396 (33.9)	379 (32.4)	0.482
ICU length of stay (day)	1.6±2.8	3.4±6.2	<0.001	1.6±2.4	2.0±4.4	0.068
Hospital length of stay (day)	5.2±8.2	9.4±23.1	<0.001	5.0±6.4	5.2±8.5	0.537
In-hospital mortality	1 (0.1)	30 (1.2)	<0.001	1 (0.1)	4 (0.3)	0.374

Values are presented as mean±standard deviation or number (%).

PWR: platelet-to-white blood cell ratio; MBP: mean blood pressure; TWA: time weighted average; KIDGO: Kidney Disease Improving Global Outcomes; ICU: intensive care unit.

^a)n=724 in high PWR group and n=1,007 in low PWR group before propensity matching and n=436 in high PWR group and n=423 in low PWR group after propensity matching.

Table 2.

Univariate and multivariate logistic regression analyses for postoperative acute kidney injury following cerebral aneurysm treatment

Variable	Before matching						After matching
	Univariate			Multivariate			Univariate
	OR	95% CI	P-value	OR	95% CI	P-value	OR	95% CI	P-value
Emergent operation	3.45	1.94–6.15	<0.001
Ruptured aneurysm	3.85	2.18–6.82	<0.001
Albumin level (g/dl)	0.38	0.19–0.77	0.007	0.47	0.23–0.95	0.035
Neutrophil count (×10⁹/L)	1.58	1.32–1.89	<0.001	1.38	1.13–1.69	0.002
Platelet count (×10⁹/L)	0.99	0.99–1.00	0.018
White blood cell count (×10⁹/L)	1.15	1.10–1.21	<0.001
Low PWR	5.01	2.25–11.13	<0.001	3.93	1.74–8.87	<0.001	3.44	1.26–9.34	0.016
Intraoperative fluid balance (ml/kg/hr)	1.07	1.03–1.11	0.002
Intraoperative transfusion	4.56	2.11–9.83	<0.001	3.27	1.47–7.31	0.004

OR: odds ratio; PWR: platelet-to-white blood cell ratio.

Table 3.

Receiver operating characteristic curve analyses of various preoperative inflammatory markers for postoperative acute kidney injury following cerebral aneurysm treatment

Variable	AUC	95% CI	P-value	P-value (vs. PWR)
Platelet-to-white blood cell ratio	0.713	0.644–0.782	<0.001	-
Neutrophil percentage-to-albumin ratio	0.671	0.592–0.750	<0.001	0.477
Neutrophil-to-lymphocyte ratio	0.648	0.569–0.728	<0.001	0.232
Platelet-to-neutrophil ratio	0.694	0.619–0.769	<0.001	0.717
Platelet-to-lymphocyte ratio	0.506	0.422–0.589	0.883	<0.001
White blood cell-to-hemoglobin ratio	0.665	0.579–0.750	<0.001	0.389
Prognostic nutritional index	0.571	0.480–0.662	0.078	0.016
Systemic inflammatory index	0.615	0.532–0.698	0.004	0.079

AUC: area under the curve; PWR: platelet-to-white blood cell ratio.

Table 4.

Comparisons of demographics, aneurysm-related data, perioperative data and clinical outcomes in patients with postoperative acute kidney injury or without following cerebral aneurysm treatment

Variable	Before matching			After matching
Variable	AKI (n=52)	Non-AKI (n=4,377)	P-value	AKI (n=22)	Non-AKI (n=2314)	P-value
Demographics
Age (yr)	58±12	59±11	0.718	59±11	59±10	0.987
Male sex	22 (42.3)	1,384 (31.6)	0.135	7 (31.8)	704 (30.4)	1.000
Body mass index (kg/m²)	24.3±3.8	24.5±3.7	0.623	24.1±3.3	24.6±3.6	0.541
Comorbidity
Hypertension	9 (17.3)	653 (14.9)	0.776	4 (18.2)	367 (15.9)	0.768
Diabetes mellitus	3 (5.8)	141 (3.2)	0.238	1 (4.5)	71 (3.1)	0.499
Pulmonary disease	0	28 (0.6)	1.000	0	14 (0.6)	1.000
Cardiac disease	1 (1.9)	99 (2.3)	1.000	0	50 (2.2)	1.000
Hepatic disease	0	48 (1.1)	1.000	0	32 (1.4)	1.000
Aneurysm-related variable
Location			0.972			0.828
Anterior	46 (88.5)	3,915 (89.4)		20 (90.9)	2,102 (90.8)
Posterior	5 (9.6)	389 (8.9)		2 (9.1)	178 (7.7)
Both	1 (1.9)	73 (1.7)		0	34 (1.5)
Number of aneurysms			0.171			0.762
1	48 (92.3)	3,715 (84.9)		20 (90.9)	1,967 (85.0)
≥2	4 (7.7)	662 (15.1)		2 (9.1)	347 (15.0)
Largest diameter of aneurysm (mm)	5.7±3.2	5.7±3.5	0.905	5.6±3.6	5.5±3.2	0.863
Emergent operation	18 (34.6)	582 (13.3)	<0.001	3 (13.6)	139 (6.0)	0.146
Recanalization	0	273 (6.2)	0.074	0	162 (7.0)	0.397
Coil embolization	38 (73.1)	3,175 (72.5)	1.000	13 (59.1)	1,676 (72.4)	0.249
Ruptured aneurysm	19 (36.5)	569 (13.0)	<0.001	2 (9.1)	120 (5.2)	0.320
Preoperative laboratory findings
Hemoglobin (g/dl)	13.2±1.9	13.2±1.5	0.959	13.0±1.4	13.2±1.4	0.612
Albumin (g/dl)	4.0±0.4	4.2±0.4	0.007	4.1±0.4	4.2±0.3	0.508
Platelet count (×10⁹/L)	219.0±54.3	238.7±60.8	0.020	204.2±53.8	236.5±65.7	0.021
Lymphocyte count (×10⁹/L)	2.1±1.3	2.1±0.9	0.930	1.9±0.6	2.1±0.6	0.184
White blood cell count (×10⁹/L)	9.4±5.1	6.9±2.9	<0.001	5.7±1.2	6.0±1.1	0.293
Neutrophil count (×10⁹/L)	0.9±1.2	0.4±0.6	0.004	0.2±0.1	0.2±0.1	0.646
PWR	28.1±11.5	38.3±13.5	<0.001	35.8±8.5	40.1±10.3	0.051
Low PWR	45 (86.5)	2,460 (56.2)	<0.001	17 (77.3)	1,151 (49.7)	0.016
Anesthetic time (hr)	3.4±1.7	3.0±1.4	0.091	4.0±2.0	3.0±1.4	0.027
Intraoperative MBP
Total time of MBP <65 mm Hg (min)	16.3±25.3	14.6±26.9	0.653	18.9±27.3	14.1±26.0	0.397
Total area of MBP <65 mm Hg (mm Hg×min)	73.6±136.6	62.6±138.1	0.568	87.8±137.8	58.2±124.3	0.267
TWA of MBP <65 mm Hg (mm Hg)	0.3±0.6	0.3±0.7	0.973	0.4±0.6	0.3±0.7	0.637
Intraoperative fluid balance (ml/kg/hr)	3.4±3.6	1.9±3.0	0.005	3.7±3.1	1.8±2.6	<0.001
Intraoperative transfusion	8 (15.4)	168 (3.8)	<0.001	5 (22.7)	82 (3.5)	0.001
Intraoperative maximum lactate (mmol/L)^a)	4.0±3.8	1.8±1.5	0.006	4.1±4.3	1.7±1.3	0.130
ICU admission	31 (59.6)	1745 (39.9)	0.006	10 (45.5)	765 (33.1)	0.317
ICU length of stay (day)	8.7±14.9	2.6±4.9	0.030	2.1±2.1	1.8±3.6	0.765
Hospital length of stay (day)	30.4±113.7	7.3±13.5	0.149	9.0±6.9	5.0±7.5	0.015
In-hospital mortality	7 (13.5)	24 (0.5)	<0.001	1 (4.5)	4 (0.2)	0.046

Values are presented as mean±standard deviation or number (%).

AKI: acute kidney injury; PWR: platelet-to-white blood cell ratio; MBP: mean blood pressure; TWA: time weighted average; ICU: intensive care unit.

^a)n=28 in AKI group and n=1,703 in non-AKI group before propensity matching, and n=9 in AKI group and n=850 in non-AKI group after propensity matching.

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A low preoperative platelet-to-white blood cell ratio is associated with acute kidney injury following cerebral aneurysm treatment in South Korea

Acute Crit Care. 2025;40(1):59-68. Published online February 21, 2025

DOI: https://doi.org/10.4266/acc.003120

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A low preoperative platelet-to-white blood cell ratio is associated with acute kidney injury following cerebral aneurysm treatment in South Korea

Figure 1. The flowchart of the study. EVD: external ventricular drainage; PWR: platelet-to-white blood cell ratio.

Figure 1.

A low preoperative platelet-to-white blood cell ratio is associated with acute kidney injury following cerebral aneurysm treatment in South Korea

Variable	Before matching			After matching
Variable	High PWR (n=1,924)	Low PWR (n=2,505)	P-value	High PWR (n=1,168)	Low PWR (n=1,168)	P-value
Demographics
Age (yr)	59±10	59±11	0.409	59±10	59±10	0.814
Male sex	421 (21.9)	985 (39.3)	<0.001	365 (31.3)	346 (29.6)	0.418
Body mass index (kg/m²)	24.4±3.6	24.6±3.7	0.079	24.5±3.5	24.6±3.8	0.735
Comorbidity
Hypertension	289 (15.0)	373 (14.9)	0.932	194 (16.6)	177 (15.2)	0.365
Diabetes mellitus	45 (2.3)	99 (4.0)	0.003	32 (2.7)	40 (3.4)	0.402
Pulmonary disease	10 (0.5)	18 (0.7)	0.450	4 (0.3)	10 (0.9)	0.178
Cardiac disease	40 (2.1)	60 (2.4)	0.541	24 (2.1)	26 (2.2)	0.886
Hepatic disease	19 (1.0)	29 (1.2)	0.662	13 (1.1)	19 (1.6)	0.373
Aneurysm-related variables
Location			0.133			0.375
Anterior	1,734 (90.1)	2,227 (88.9)		1,067 (91.4)	1,055 (90.3)
Posterior	154 (8.0)	240 (9.6)		82 (7.0)	98 (8.4)
Both	36 (1.9)	38 (1.5)		19 (1.6)	15 (1.3)
Number of aneurysms			0.734			0.908
1	1,639 (85.2)	2,124 (84.8)		995 (85.2)	992 (84.9)
≥2	285 (14.8)	381 (15.2)		173 (14.8)	176 (15.1)
Largest diameter of aneurysm (mm)	5.5±3.5	5.8±3.5	0.009	5.4±3.1	5.6±3.3	0.272
Emergent operation	98 (5.1)	502 (20.0)	<0.001	65 (5.6)	77 (6.6)	0.341
Recanalization	119 (6.2)	154 (6.1)	1.000	71 (6.1)	91 (7.8)	0.122
Coil embolization	1,366 (71.0)	1,847 (73.7)	0.045	840 (71.9)	849 (72.7)	0.711
Ruptured aneurysm	82 (4.3)	506 (20.0)	<0.001	60 (5.1)	62 (5.3)	0.926
Preoperative laboratory findings
Hemoglobin (g/dl)	12.9±1.4	13.4±1.5	<0.001	13.2±1.4	13.1±1.4	0.367
Albumin (g/dl)	4.2±0.3	4.1±0.4	<0.001	4.2±0.3	4.2±0.3	0.313
Platelet count (×10⁹/L)	262.7±59.3	219.9±55.0	<0.001	277.9±58.7	194.6±41.3	<0.001
Lymphocyte count (×10⁹/L)	1.9±0.6	2.2±1.0	<0.001	2.1±0.6	2.1±0.6	0.832
White blood cell count (×10⁹/L)	5.4±1.2	8.1±3.4	<0.001	5.9±1.1	6.0±1.1	0.017
Neutrophil count (×10⁹/L)	0.2±0.1	0.5±0.7	<0.001	0.2±0.1	0.2±0.1	0.053
PWR	49.8±10.8	29.3±7.0	<0.001	47.6±8.6	32.5±4.9	<0.001
Anesthetic time (hr)	2.9±1.4	3.1±1.5	<0.001	2.9±1.4	3.0±1.5	0.088
Intraoperative MBP
Total time of MBP <65 mm Hg (min)	12.0±22.8	16.5±29.5	<0.001	12.8±23.8	15.6±28.0	0.008
Total area of MBP <65 mm Hg (mm Hg×min)	50.4±114.5	72.2±153.1	<0.001	52.4±117.3	64.7±131.0	0.017
TWA of MBP <65 mm Hg (mm Hg)	0.3±0.6	0.4±0.8	<0.001	0.3±0.6	0.4±0.7	0.037
Intraoperative fluid balance (ml/kg/hr)	1.7±2.5	2.1±3.3	<0.001	1.8±2.5	1.9±2.7	0.208
Intraoperative transfusion	64 (3.3)	112 (4.5)	0.064	34 (2.9)	53 (4.5)	0.049
Intraoperative maximum lactate (mmol/L)^a)	1.6±1.2	2.0±1.8	<0.001	1.7±1.2	1.7±1.5	0.574
Acute kidney injury	7 (0.4)	45 (1.8)	<0.001	5 (0.4)	17 (1.5)	0.016
KIDGO stage 1:2:3	6:1:0	42:2:1		4:1:0	17:0:0
ICU admission	664 (34.5)	1,112 (44.4)	<0.001	396 (33.9)	379 (32.4)	0.482
ICU length of stay (day)	1.6±2.8	3.4±6.2	<0.001	1.6±2.4	2.0±4.4	0.068
Hospital length of stay (day)	5.2±8.2	9.4±23.1	<0.001	5.0±6.4	5.2±8.5	0.537
In-hospital mortality	1 (0.1)	30 (1.2)	<0.001	1 (0.1)	4 (0.3)	0.374

Variable	Before matching						After matching
	Univariate			Multivariate			Univariate
	OR	95% CI	P-value	OR	95% CI	P-value	OR	95% CI	P-value
Emergent operation	3.45	1.94–6.15	<0.001
Ruptured aneurysm	3.85	2.18–6.82	<0.001
Albumin level (g/dl)	0.38	0.19–0.77	0.007	0.47	0.23–0.95	0.035
Neutrophil count (×10⁹/L)	1.58	1.32–1.89	<0.001	1.38	1.13–1.69	0.002
Platelet count (×10⁹/L)	0.99	0.99–1.00	0.018
White blood cell count (×10⁹/L)	1.15	1.10–1.21	<0.001
Low PWR	5.01	2.25–11.13	<0.001	3.93	1.74–8.87	<0.001	3.44	1.26–9.34	0.016
Intraoperative fluid balance (ml/kg/hr)	1.07	1.03–1.11	0.002
Intraoperative transfusion	4.56	2.11–9.83	<0.001	3.27	1.47–7.31	0.004

Variable	AUC	95% CI	P-value	P-value (vs. PWR)
Platelet-to-white blood cell ratio	0.713	0.644–0.782	<0.001	-
Neutrophil percentage-to-albumin ratio	0.671	0.592–0.750	<0.001	0.477
Neutrophil-to-lymphocyte ratio	0.648	0.569–0.728	<0.001	0.232
Platelet-to-neutrophil ratio	0.694	0.619–0.769	<0.001	0.717
Platelet-to-lymphocyte ratio	0.506	0.422–0.589	0.883	<0.001
White blood cell-to-hemoglobin ratio	0.665	0.579–0.750	<0.001	0.389
Prognostic nutritional index	0.571	0.480–0.662	0.078	0.016
Systemic inflammatory index	0.615	0.532–0.698	0.004	0.079

Variable	Before matching			After matching
Variable	AKI (n=52)	Non-AKI (n=4,377)	P-value	AKI (n=22)	Non-AKI (n=2314)	P-value
Demographics
Age (yr)	58±12	59±11	0.718	59±11	59±10	0.987
Male sex	22 (42.3)	1,384 (31.6)	0.135	7 (31.8)	704 (30.4)	1.000
Body mass index (kg/m²)	24.3±3.8	24.5±3.7	0.623	24.1±3.3	24.6±3.6	0.541
Comorbidity
Hypertension	9 (17.3)	653 (14.9)	0.776	4 (18.2)	367 (15.9)	0.768
Diabetes mellitus	3 (5.8)	141 (3.2)	0.238	1 (4.5)	71 (3.1)	0.499
Pulmonary disease	0	28 (0.6)	1.000	0	14 (0.6)	1.000
Cardiac disease	1 (1.9)	99 (2.3)	1.000	0	50 (2.2)	1.000
Hepatic disease	0	48 (1.1)	1.000	0	32 (1.4)	1.000
Aneurysm-related variable
Location			0.972			0.828
Anterior	46 (88.5)	3,915 (89.4)		20 (90.9)	2,102 (90.8)
Posterior	5 (9.6)	389 (8.9)		2 (9.1)	178 (7.7)
Both	1 (1.9)	73 (1.7)		0	34 (1.5)
Number of aneurysms			0.171			0.762
1	48 (92.3)	3,715 (84.9)		20 (90.9)	1,967 (85.0)
≥2	4 (7.7)	662 (15.1)		2 (9.1)	347 (15.0)
Largest diameter of aneurysm (mm)	5.7±3.2	5.7±3.5	0.905	5.6±3.6	5.5±3.2	0.863
Emergent operation	18 (34.6)	582 (13.3)	<0.001	3 (13.6)	139 (6.0)	0.146
Recanalization	0	273 (6.2)	0.074	0	162 (7.0)	0.397
Coil embolization	38 (73.1)	3,175 (72.5)	1.000	13 (59.1)	1,676 (72.4)	0.249
Ruptured aneurysm	19 (36.5)	569 (13.0)	<0.001	2 (9.1)	120 (5.2)	0.320
Preoperative laboratory findings
Hemoglobin (g/dl)	13.2±1.9	13.2±1.5	0.959	13.0±1.4	13.2±1.4	0.612
Albumin (g/dl)	4.0±0.4	4.2±0.4	0.007	4.1±0.4	4.2±0.3	0.508
Platelet count (×10⁹/L)	219.0±54.3	238.7±60.8	0.020	204.2±53.8	236.5±65.7	0.021
Lymphocyte count (×10⁹/L)	2.1±1.3	2.1±0.9	0.930	1.9±0.6	2.1±0.6	0.184
White blood cell count (×10⁹/L)	9.4±5.1	6.9±2.9	<0.001	5.7±1.2	6.0±1.1	0.293
Neutrophil count (×10⁹/L)	0.9±1.2	0.4±0.6	0.004	0.2±0.1	0.2±0.1	0.646
PWR	28.1±11.5	38.3±13.5	<0.001	35.8±8.5	40.1±10.3	0.051
Low PWR	45 (86.5)	2,460 (56.2)	<0.001	17 (77.3)	1,151 (49.7)	0.016
Anesthetic time (hr)	3.4±1.7	3.0±1.4	0.091	4.0±2.0	3.0±1.4	0.027
Intraoperative MBP
Total time of MBP <65 mm Hg (min)	16.3±25.3	14.6±26.9	0.653	18.9±27.3	14.1±26.0	0.397
Total area of MBP <65 mm Hg (mm Hg×min)	73.6±136.6	62.6±138.1	0.568	87.8±137.8	58.2±124.3	0.267
TWA of MBP <65 mm Hg (mm Hg)	0.3±0.6	0.3±0.7	0.973	0.4±0.6	0.3±0.7	0.637
Intraoperative fluid balance (ml/kg/hr)	3.4±3.6	1.9±3.0	0.005	3.7±3.1	1.8±2.6	<0.001
Intraoperative transfusion	8 (15.4)	168 (3.8)	<0.001	5 (22.7)	82 (3.5)	0.001
Intraoperative maximum lactate (mmol/L)^a)	4.0±3.8	1.8±1.5	0.006	4.1±4.3	1.7±1.3	0.130
ICU admission	31 (59.6)	1745 (39.9)	0.006	10 (45.5)	765 (33.1)	0.317
ICU length of stay (day)	8.7±14.9	2.6±4.9	0.030	2.1±2.1	1.8±3.6	0.765
Hospital length of stay (day)	30.4±113.7	7.3±13.5	0.149	9.0±6.9	5.0±7.5	0.015
In-hospital mortality	7 (13.5)	24 (0.5)	<0.001	1 (4.5)	4 (0.2)	0.046

Table 1. Comparisons of demographics, aneurysm-related data, perioperative data and clinical outcomes in patients with high or low preoperative platelet-to-white blood cell ratio who underwent cerebral aneurysm treatment

Values are presented as mean±standard deviation or number (%).

PWR: platelet-to-white blood cell ratio; MBP: mean blood pressure; TWA: time weighted average; KIDGO: Kidney Disease Improving Global Outcomes; ICU: intensive care unit.

n=724 in high PWR group and n=1,007 in low PWR group before propensity matching and n=436 in high PWR group and n=423 in low PWR group after propensity matching.

Table 2. Univariate and multivariate logistic regression analyses for postoperative acute kidney injury following cerebral aneurysm treatment

OR: odds ratio; PWR: platelet-to-white blood cell ratio.

Table 3. Receiver operating characteristic curve analyses of various preoperative inflammatory markers for postoperative acute kidney injury following cerebral aneurysm treatment

AUC: area under the curve; PWR: platelet-to-white blood cell ratio.

Table 4. Comparisons of demographics, aneurysm-related data, perioperative data and clinical outcomes in patients with postoperative acute kidney injury or without following cerebral aneurysm treatment

Values are presented as mean±standard deviation or number (%).

AKI: acute kidney injury; PWR: platelet-to-white blood cell ratio; MBP: mean blood pressure; TWA: time weighted average; ICU: intensive care unit.

n=28 in AKI group and n=1,703 in non-AKI group before propensity matching, and n=9 in AKI group and n=850 in non-AKI group after propensity matching.