# Association between serum glucose/potassium ratio and acute kidney injury in patients with traumatic brain injury: based on MIMIC-IV database

## TL;DR

This study finds that higher glucose-to-potassium ratio in blood is linked to increased risk of kidney injury in traumatic brain injury patients.

## Contribution

Identifies serum glucose-to-potassium ratio as a novel biomarker for predicting acute kidney injury in traumatic brain injury patients.

## Key findings

- Each unit increase in GPR raises AKI risk by 1.3% in TBI patients.
- Fluid balance partially mediates the GPR-AKI relationship in TBI patients.
- Subgroup analysis shows significant AKI risk correlation in patients with abnormal glucose or normal potassium levels.

## Abstract

Acute kidney injury (AKI) is a common complication in patients with traumatic brain injury (TBI) and is closely linked to prognosis. Although the serum glucose-to-potassium ratio (GPR) is a prognostic indicator in various diseases, its clinical significance in this specific patient population remains unexplored.

We identified patients requiring intensive care unit admission from the critical care medical information database and stratified them into quintiles based on GPR. The nonlinear relationship between GPR and AKI in TBI patients was analysed by restricted cubic splines (RCS). We conducted an exploratory subgroup analysis to investigate the differences in this association across different subgroups. Using mediation analysis, we aimed to explore the potential mediating effect of fluid balance in the development of AKI in patients with GPR and TBI.

1536 patients with TBI were included, of whom 1162 developed AKI. Every one unit increase in GPR increases the risk of AKI in TBI patients by 1.3% (odds ratio (OR) = 1.013; 95% confidence interval CI) = 1.004–1.024, P = 0.014). Further, RCS analysis indicated an approximately linear positive correlation between the increase in GPR and the AKI risk (P = 0.235). Subgroup analysis indicated that both patients with abnormal serum glucose and those with normal potassium levels showed a significant positive correlation with AKI risk (OR>1, P < 0.05). Fluid balance potentially mediated the association between GPR and TBI-induced AKI in part, with a mediating effect of 4.49 × 10−4 (95% CI = 2.04 × 10−4–1.18 × 10−3, P < 0.001).

GPR is significantly associated with AKI risk in TBI patients, which may be mediated by FB. We identified GPR as a new biomarker for assessing AKI risk in TBI patients, thereby offering fresh insights into prevention and treatment for this population.