Impact of AKI on metabolic compensation for respiratory acidosis in ICU patients with AECOPD

Purpose

Acute exacerbation of chronic obstructive pulmonary disease (AECOPD) can result in severe respiratory acidosis. Metabolic compensation is primarily achieved by renal retention of bicarbonate. The extent to which acute kidney injury (AKI) impairs the kidney's capacity to compensate for respiratory acidosis remains unclear.

Materials and methods

This retrospective analysis covers clinical data between January 2009 and December 2021 for 498 ICU patients with AECOPD and need for respiratory support.

Results

278 patients (55.8%) presented with or developed AKI. Patients with AKI exhibited higher 30-day-mortality rates (14.5% vs. 4.5% p = 0.001), longer duration of mechanical ventilation (median 90 h vs. 14 h; p = 0.001) and more severe hypercapnic acidosis (pH 7.23 vs. 7.28; pCO₂ 68.5 mmHg vs. 61.8 mmHg). Patients with higher AKI stages exhibited lower HCO₃⁻/pCO₂ ratios and did not reach expected HCO₃⁻ levels. In a mixed model analysis with random intercept per patient we analyzed the association of pCO₂ (independent) and HCO₃⁻ (dependent variable). Lower estimates for averaged change in HCO₃⁻ were observed in patients with more severe AKI.

Conclusion

AKI leads to poor outcomes and compromises metabolic compensation of respiratory acidosis in ICU patients with AECOPD. While buffering agents may aid compensation for severe AKI, their use should be approached with caution.