Abstract
BACKGROUND: Sepsis has long been a life-threatening organ dysfunction. Sepsis associated acute kidney injury (SA-AKI) is an important complication of sepsis, as an important hemodynamic index, the impact of central venous pressure (CVP) on sepsis patients needs to be explored. Thus this study aimed to investigate the relationship between CVP and the mortality of SA-AKI. METHODS: Clinical data of adult patients with sepsis-related acute kidney injury, defined as met both the Sepsis 3.0 criteria and the Kidney Disease Improving Global Outcomes Clinical Practice Guideline (KDIGO) criteria, were obtained from the Medical Information Mart for Intensive Care-IV (MIMIC-IV) database. The included cohort was divided into a high CVP and a low CVP group were determined based on the cuf-off value from receiver operating characteristic curve, with propensity score-matched analysis of the 28-day mortality for both groups and sensitivity analysis using inverse the probability-weighting model, multifactorial regression, and doubly robust estimation, patients acquired chronic coronary syndrome (CCS) and diabetes were also taken into consideration. RESULTS: Of 1,377 patients with sepsis-related acute kidney injury, low CVP group (<13 mmHg) was 67.4% (n=928) and high CVP group (≥13 mmHg) was 32.6% (n=449). The two groups were matched 1:1 by propensity score to obtain a matched cohort (n=288). The mortality rates in the low versus high CVP group (19.4% vs. 34.7%) were statistically difference (odds ratio OR: 0.454; 95% confidence interval 0.263, 0.771). Moreover, the bistable analysis of logistic regression of the matched cohort (OR: 0.434; 95% CI: 0.244, 0.757), propensity score inverse probability weighting (IPW) (OR: 0.547; 95% CI: 0.454, 0.658), and multifactorial logistic regression (OR: 0.352; 95% CI: 0.127, 0.932) all yielded the same results. CONCLUSIONS: In patients with sepsis-related acute kidney injury, a lower CVP level (<13 mmHg) is an independent variable associated with decreased mortality. The threshold of CVP needs to be controlled in clinical work to improve the prognosis of patients with SA-AKI.