Impact of AKI on metabolic compensation for respiratory acidosis in ICU patients with AECOPD.
- Resource Type
- Academic Journal
- Authors
- Marcy F; Charité - Universitätsmedizin Berlin, Department of Nephrology and Medical Intensive Care Medicine, Berlin, Germany. Electronic address: florian.marcy@charite.de.; Goettfried K; Charité - Universitätsmedizin Berlin, Department of Nephrology and Medical Intensive Care Medicine, Berlin, Germany.; Enghard P; Charité - Universitätsmedizin Berlin, Department of Nephrology and Medical Intensive Care Medicine, Berlin, Germany.; Piper SK; Charité - Universitätsmedizin Berlin, Institute of Biometry and Clinical Epidemiology, Berlin, Germany; Berlin Institute of Health (BIH), Anna-Louisa-Karsch-Strasse 2, 10178 Berlin, Germany; Charité - Universitätsmedizin Berlin, Institute of Medical Informatics Berlin, Germany.; Kunz JV; Charité - Universitätsmedizin Berlin, Department of Nephrology and Medical Intensive Care Medicine, Berlin, Germany.; Schroeder T; Charité - Universitätsmedizin Berlin, Department of Nephrology and Medical Intensive Care Medicine, Berlin, Germany.
- Source
- Publisher: W.B. Saunders Country of Publication: United States NLM ID: 8610642 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1557-8615 (Electronic) Linking ISSN: 08839441 NLM ISO Abbreviation: J Crit Care Subsets: MEDLINE
- Subject
- Language
- English
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; pCO 2 68.5 mmHg vs. 61.8 mmHg). Patients with higher AKI stages exhibited lower HCO 3 - /pCO 2 ratios and did not reach expected HCO 3 - levels. In a mixed model analysis with random intercept per patient we analyzed the association of pCO 2 (independent) and HCO 3 - (dependent variable). Lower estimates for averaged change in HCO 3 - 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.
Competing Interests: Declaration of competing interest The authors have disclosed that they do not have any conflicts of interest. The authors did not receive funding for this study.
(Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.)