# Normalization of elevated preoperative serum creatinine and acute kidney injury after cardiac surgery: a retrospective cohort study

**Authors:** Bo Jiang, Genshen Zhen, Haiping Yang, Yi Hao, Meiping Wang, Zhenhua Zhang, Lin Chen, Ning He, Yueling Chen, Li Jiang

PMC · DOI: 10.1038/s41598-025-13719-4 · Scientific Reports · 2025-07-31

## TL;DR

This study finds that normalizing elevated preoperative kidney function before heart surgery is linked to a higher risk of kidney injury afterward.

## Contribution

The study introduces a novel categorization of preoperative creatinine changes and shows their impact on postoperative acute kidney injury outcomes.

## Key findings

- Normalized preoperative serum creatinine was associated with increased risk of acute kidney injury (AKI) after surgery.
- Patients with normalized creatinine had higher rates of severe and persistent AKI compared to those with stable creatinine.
- Propensity score matching confirmed the increased AKI risk in the normalized creatinine group.

## Abstract

Preoperative kidney dysfunction is a predictor of acute kidney injury (AKI) following cardiac surgery, limited information exists regarding the impact of preoperative serum creatinine (sCr) change on AKI. This study aims to examine the association between the normalization of elevated preoperative sCr and postoperative AKI, as well as its severity and duration. This retrospective cohort study included patients undergoing open-heart surgery. Patients were categorized into three groups based on preoperative sCr change (ΔScr): the Stable sCr group (maximum ΔScr < 0.3 mg/dL throughout the preoperative period), the Normalized sCr group (maximum ΔScr ≥ 0.3 mg/dL followed by normalization to < 0.3 mg/dL within 48 h pre-surgery), and the Worsened sCr group (maximum ΔScr ≥ 0.3 mg/dL, remaining ≥ 0.3 mg/dL within 48 h pre-surgery). Multivariable logistic regression was used to evaluate the association between preoperative sCr change and postoperative AKI, severe AKI, and persistent AKI. To control for selection bias, propensity score matching (1:3) was used by matching covariates between the Normalized sCr and the Stable sCr group. Of the 560 patients included, 40.2% developed AKI. In the Normalized sCr group, the rate of AKI was 61.2%, severe AKI 22.4%, and persistent AKI 34.7%. Multivariable logistic regression analyses revealed the Normalized group was associated with higher risk of postoperative AKI (adjusted OR, 2.51; 95% CI, 1.30‒4.85, p = 0.006), severe AKI (adjusted OR, 3.40; 95% CI, 1.37–8.45, p = 0.008) and persistent AKI (adjusted OR, 2.87; 95% CI 1.36‒6.05, p = 0.006). After propensity matching, 184 patients were matched (46 in the Normalized sCr group and 138 in the Stable sCr group). The Normalized sCr group were still associated with risk of AKI (adjusted OR, 2.77; 95% CI, 1.34–5.73, p = 0.006), severe AKI (adjusted OR, 4.10; 95% CI, 1.32–12.71, p = 0.015) and persistent AKI (adjusted OR, 2.72; 95% CI, 1.21–6.15, p = 0.016). Normalization of preoperative sCr following an initial elevation was associated with higher risks of AKI, as well as AKI severity and duration.

The online version contains supplementary material available at 10.1038/s41598-025-13719-4.

## Linked entities

- **Diseases:** acute kidney injury (MONDO:0002492)

## Full-text entities

- **Genes:** LCN2 (lipocalin 2) [NCBI Gene 3934] {aka 24p3, MSFI, NGAL, p25}, HAVCR1 (hepatitis A virus cellular receptor 1) [NCBI Gene 26762] {aka CD365, HAVCR, HAVCR-1, KIM-1, KIM1, TIM}
- **Diseases:** kidney damage (MESH:D007674), NYHA (MESH:D006331), AKI (MESH:D058186), diabetes mellitus (MESH:D003920), inflammatory drugs (MESH:D000081015), anuria (MESH:D001002), infection (MESH:D007239), hypertension (MESH:D006973), inflammation (MESH:D007249), venous congestion (MESH:D006940), sCr (MESH:D012713), CKD (MESH:D051436), heart failure (MESH:D006333)
- **Chemicals:** ACEIs (-), creatinine (MESH:D003404)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

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## References

2 references — full list in the complete paper: https://tomesphere.com/paper/PMC12313847/full.md

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Source: https://tomesphere.com/paper/PMC12313847