Background: Serum lactate level has been confirmed to be an independent risk factor for the occurrence of acute kidney injury (AKI) in many diseases. However, the correlation between serum lactate level and AKI in critical patients with acute ischemic stroke (AIS) has not been unclear. Moreover, limited studies have examined the mediating effect of serum glucose on the association between Serum lactate and AKI.
Methods: We identified 1,435 AIS patients from the Medical Information Mart for Intensive Care (MIMIC-III) database and divided them into AKI or No-AKI groups. We used a propensity score matching (PSM) method to reduce confounding. Linear regression, logistic regression, and restricted cubic splines (RCS) were used to evaluate relationships between blood lactate levels and serum glucose, serum lactate, as well as AKI. Finally, the mediating role of serum glucose on the relationship between serum lactate and AKI was investigated utilizing the mediation analysis.
Results: In the present study, a total of 634 critical patients with AIS aged ≥18 years were included after propensity score matching (1:1). we use RCS plot to reveal a linear association of between serum lactate levels and AKI and between serum glucose levels and serum lactate levels (all P for nonlinear <0.001). After full adjustment for potential confounders (Model 3), serum glucose was positively correlated to serum lactate level (β=0.004, 95% CI: 0.003-0.006, P-value <0.001). High lactate level increased the risk of AKI (OR, 2.216; 95% CI, 1.559-3.271; P-value <0.001). Serum glucose explained 14.9% of the association between serum lactate and AKI among critical patients with AIS (P-value <0.001), 16.4% among patients with AIS and DM (P-value =0.24), and 19.5% among patients with AIS and without DM (P-value <0.001).
Conclusion: Serum lactate acid was independently associated with increased risk-adjusted AKI in critical patients with AIS. The increase in serum glucose may have mediated this effect, especially in patients without DM.