Iron metabolism-related indicators as predictors of the incidence of acute kidney injury after cardiac surgery: a meta-analysis

Abstract

Background: Some studies have found that ferroptosis plays an important role in the incidence of acute kidney injury (AKI) after cardiac surgery. However, whether iron metabolism-related indicators can be used as predictors of the incidence of AKI after cardiac surgery remains unclear.

Objectives: We aimed to systematically evaluate whether iron metabolism-related indicators can be used as predictors of the incidence of AKI after cardiac surgery via meta-analysis.Search methods: The PubMed, Embase, Web of Science, and Cochrane Library databases were searched from January 1971 to February 2023 to identify prospective observational and retrospective observational studies examining iron metabolism-related indicators and the incidence of AKI after cardiac surgery among adults.Data Extraction and Synthesis: The following data were extracted by two independent authors (ZLM and YXY): date of publication, first author, country, age, sex, number of included patients, iron metabolism-related indicators, outcomes of patients, patient types, study types, sample, and specimen sampling time. The level of agreement between authors was determined using Cohen's κ value. The Newcastle-Ottawa Scale (NOS) was used to evaluate the quality of studies. Statistical heterogeneity across the studies was measured by the I² statistic. The standardized mean difference (SMD) and 95% confidence interval (CI) were used as effect size measures. Meta-analysis was performed using Stata 15.

Results: After applying the inclusion and exclusion criteria, 9 articles on iron metabolism-related indicators and the incidence of AKI after cardiac surgery were included in this study. Meta-analysis revealed that after cardiac surgery, baseline serum ferritin (μg/L) (I² = 43%, fixed effects model, SMD = -0.3, 95% CI:-0.54 to -0.07, p = 0.010), preoperative and 6-hour postoperative fractional excretion (FE) of hepcidin (%) (I² = 0.0%, fixed effects model, SMD = -0.41, 95% CI: -0.79 to -0.02, p = 0.038; I² = 27.0%, fixed effects model, SMD = -0.49, 95% CI: -0.88 to -0.11, p = 0.012), 24-hour postoperative urinary hepcidin (μg/L) (I² = 0.0%, fixed effects model, SMD = -0.60, 95% CI: -0.82 to -0.37, p < 0.001) and urine hepcidin/urine creatinine ratio (μg/mmoL) (I² = 0.0%, fixed effects model, SMD = -0.65, 95% CI: -0.86 to -0.43, p < 0.001) were significantly lower in patients who developed to AKI than in those who did not.

Conclusion: After cardiac surgery, patients with lower baseline serum ferritin levels (μg/L), lower preoperative and 6-hour postoperative FE of hepcidin (%), lower 24-hour postoperative hepcidin/urine creatinine ratios (μg/mmol) and lower 24-hour postoperative urinary hepcidin levels (μg/L) are more likely to develop AKI. Therefore, these parameters have the potential to be predictors for AKI after cardiac surgery in the future. In addition, there is a need for relevant clinical research of larger scale and with multiple centers to further test these parameters and prove our conclusion.Trial Registration: PROSPERO identifier: CRD42022369380.

Keywords: Iron metabolism; acute kidney injury; cardiac surgery; incidence; meta-analysis.

Figure 1.

Flowchart of study selection.

Figure 2.

Forest plot of the incidence of acute kidney injury after cardiac surgery and serum ferritin. Forest plot revealing that patients who developed AKI after cardiac surgery had lower baseline serum ferritin levels than those who did not develop AKI (p = 0.010). 95% CI, 95% confidence interval.

Figure 3.

Forest plot of the incidence of acute kidney injury after cardiac surgery and plasma hepcidin. Forest plot indicating no significant difference in plasma hepcidin levels between patients undergoing cardiac surgery who developed AKI and those who did not (p = 0.416; p = 0.539). 95% CI, 95% confidence interval.

Figure 4.

Forest plot of the incidence of acute kidney injury after cardiac surgery and urinary hepcidin. Forest plot showing that after cardiac surgery, the level of 24-h postoperative urinary hepcidin in patients who developed AKI was lower than that in patients who did not develop AKI (p = 0.000); however, preoperative and 6-h postoperative urinary hepcidin levels were not significantly different between patients who developed AKI and those who did not develop AKI (p = 0.254; p = 0.542). 95% CI, 95% confidence interval.

Figure 5.

Forest plot of the incidence of acute kidney injury after cardiac surgery and urinary hepcidin/urine creatinine ratio. Forest plot indicating that patients who developed AKI after cardiac surgery had a lower 24-h postoperative urinary hepcidin/urine creatinine ratio than those who did not develop AKI after cardiac surgery (p = 0.000); however, there was no significant difference in the 6-h postoperative urinary hepcidin/urine creatinine ratio between patients who developed AKI and those who did not develop AKI (p = 0.377). 95% CI, 95% confidence interval.

Figure 6.

Forest plot of the incidence of acute kidney injury after cardiac surgery and urinary FE of hepcidin. Forest plot displaying that the levels of preoperative and 6-h postoperative urine FE of hepcidin (p = 0.038; p = 0.012) in patients who developed AKI after cardiac surgery were lower than those in patients who did not develop AKI after cardiac surgery; however, there was no significant difference in the levels of 24-h postoperative FE of hepcidin between patients who developed AKI after cardiac surgery and those who did not develop AKI after cardiac surgery (p = 0.726). 95% CI, 95% confidence interval.