Association between dynamic estimated plasma volume trajectories and acute kidney injury after coronary artery bypass grafting.

Authors

Beijun Gao, Hongmin Zhang, Ran An, Nan Cheng, Xin Wu, Xianqiang Wang, Juan Du

Published in

Frontiers in medicine. Volume 13. Pages 1912347. Epub Sep 09, 2026.

Abstract

Cardiac surgery-associated acute kidney injury (CSA-AKI) is driven partly by venous congestion, yet no single bedside measure fully captures volume status: central venous pressure (CVP) reflects venous pressure, not plasma-volume expansion. Whether dynamic estimated plasma volume status (ePVS), a non-invasive marker derived from routine hemoglobin and hematocrit, conveys AKI-relevant information independent of and complementary to CVP is unknown.
In 4,818 adult patients with coronary artery bypass grafting (CABG) from Medical Information Mart for Intensive Care IV, version 3.0 (MIMIC-IV v3.0), serial ePVS over the first 48 h after admission to the intensive care unit (ICU) was modeled by latent-class linear mixed modeling to identify dynamic phenotypes. The primary outcome was Kidney Disease: Improving Global Outcomes (KDIGO) acute kidney injury (AKI) stage ≥ 2 within 72 h. Independence from CVP was tested by the ePVS-CVP correlation, progressive adjustment for admission CVP, CVP-stratified analysis with a trajectory by CVP interaction term, and parallel multiple-mediator analysis (24-h ΔHgb, peak CVP, net fluid balance). Forward-time landmark analyses and incremental-value metrics [Δ area under the curve (ΔAUC), net reclassification improvement (NRI), integrated discrimination improvement (IDI), and decision-curve analysis] were also performed.
Four phenotypes emerged: Low-stable (58.5%), Gradually-increasing (6.9%), Rapid-decline (8.7%), and High-stable (25.9%). Admission ePVS and CVP were essentially uncorrelated (Spearman r = 0.04), indicating non-redundant axes. Only the Gradually-increasing phenotype was independently associated with AKI (Model 3 OR 1.47, 95% CI 1.14 to 1.89), and this was barely changed by adjustment for admission CVP (from 1.58 in Model 1 to 1.49 in Model 2); peak CVP mediated only 9.9% of the total effect, the majority not being attributable to any single measured pathway. Forward-time landmarking amplified the association (OR 2.10 at 24 h; 2.26 at 48 h), arguing against reverse causation. The trajectory-by-CVP interaction was not significant (p = 0.20); the phenotype effect was numerically larger at low than high admission CVP (OR 1.76 versus 1.20), an exploratory pattern. Adding trajectory class to a static model produced modest gains (NRI 9.9%, IDI 0.4%, ΔAUC 0.003).
Four distinct ePVS trajectories within 48 h after CABG carry differential AKI risk. A Gradually-increasing ePVS trajectory after CABG signifies AKI risk that is largely independent of and complementary to CVP, providing a non-invasive volume axis not captured by pressure-based monitoring.

PMID:
42780204
Bibliographic data and abstract were imported from PubMed on 24 Sep 2026.

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