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Impact of AKI on metabolic compensation for respiratory acidosis in ICU patients with AECOPD.
Marcy, Florian; Goettfried, Katharina; Enghard, Philipp; Piper, Sophie K; Kunz, Julius Valentin; Schroeder, Tim.
Afiliación
  • 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.
J Crit Care ; 83: 154846, 2024 Oct.
Article en En | MEDLINE | ID: mdl-38936337
ABSTRACT

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.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Acidosis Respiratoria / Enfermedad Pulmonar Obstructiva Crónica / Lesión Renal Aguda / Unidades de Cuidados Intensivos Límite: Aged / Female / Humans / Male / Middle aged Idioma: En Revista: J Crit Care Asunto de la revista: TERAPIA INTENSIVA Año: 2024 Tipo del documento: Article Pais de publicación: Estados Unidos
Texto completo
Añadir a Mi BVS
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XML
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Acidosis Respiratoria / Enfermedad Pulmonar Obstructiva Crónica / Lesión Renal Aguda / Unidades de Cuidados Intensivos Límite: Aged / Female / Humans / Male / Middle aged Idioma: En Revista: J Crit Care Asunto de la revista: TERAPIA INTENSIVA Año: 2024 Tipo del documento: Article Pais de publicación: Estados Unidos