Fine-Mapping the Association of Acute Kidney Injury With Mean Arterial and Central Venous Pressures During Coronary Artery Bypass Surgery.
Summary
Among 1,199 CABG patients, AKI risk decreased in MAP 90–95 mmHg and CVP 4–6 mmHg ranges and in joint exposures with MAP >75 and CVP <8. The analysis challenges current guideline targets (MAP >65; CVP 8–12), showing no protective signal within those ranges.
Key Findings
- AKI risk increased with time spent at MAP 45–60 mmHg and decreased at MAP 90–95 mmHg (aOR 0.85; P<.001).
- AKI risk decreased in CVP 4–6 mmHg (aOR 0.97; P=.025) and increased in CVP 16–18 mmHg (aOR 1.07; P=.002).
- Joint analysis showed protection with MAP >75 mmHg and CVP <8 mmHg across zones; no protective signal for MAP 65–75 or CVP 8–12.
Clinical Implications
During CABG, consider targeting higher MAP (≈90–95 mmHg) while avoiding venous congestion (CVP ≈4–6 mmHg; <8) rather than relying on MAP 65–75 or CVP 8–12. Incorporate joint MAP/CVP monitoring and protocols; validate prospectively before broad adoption.
Why It Matters
Defines narrow, actionable hemodynamic target zones using joint MAP/CVP exposure, offering an evidence base to refine intraoperative kidney-protective strategies.
Limitations
- Retrospective, single-procedure cohort limits causal inference and generalizability beyond CABG.
- Residual confounding (e.g., fluid status, vasopressor selection) cannot be fully excluded.
Future Directions
Prospective RCTs testing joint MAP/CVP targets; integration into closed-loop hemodynamic management; exploration of individualized targets by renal risk phenotypes.
Study Information
- Study Type
- Cohort
- Research Domain
- Prognosis
- Evidence Level
- III - Retrospective cohort with multivariable exposure-response mapping for intraoperative hemodynamics and AKI.
- Study Design
- OTHER