Factors associated with acute kidney injury in acute respiratory distress syndrome

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Abstract

Background

Acute kidney injury (AKI) is the most frequent extra-pulmonary organ failure in acute respiratory distress syndrome (ARDS). The objective of this study was to assess the factors associated with the development and severity of AKI in patients with ARDS.

Methods

This is a retrospective cohort study of ARDS patients without acute or chronic kidney disease prior to the onset of ARDS over a 7-year period (2010–2017). AKI and severity of AKI were defined according to the Kidney Disease Improving Global Outcomes 2012 guidelines.

Results

Of the 634 ARDS patients, 357 patients met study criteria. A total of 244 (68.3%) patients developed AKI after ARDS onset: 60 (24.6%) had stage I AKI, 66 (27%) had stage II AKI, and 118 (48.4%) had stage III AKI. The median time of AKI onset for stage I AKI was 2 days (interquartile range, 1.5–5.5) while stage II and III AKI was 4 days. On multivariable analysis, factors associated with development of AKI were age [subdistribution hazard ratio (SHR) 1.01, 95% confidence interval (CI) 1.00–1.02], SOFA score (SHR 1.16, 95%CI 1.12–1.21), a history of diabetes mellitus (DM) (SHR 1.42, 95%CI 1.07–1.89), and arterial pH on day 1 of ARDS (SHR per 0.1 units decrease was 1.18, 95%CI 1.05–1.32). In severity of AKI, stage I AKI was associated with age (SHR 1.03, 95%CI 1.01–1.05) and serum bicarbonate on day 1 of ARDS (SHR 1.07, 95%CI 1.02–1.13). Stage II AKI was associated with age (SHR 1.03, 95%CI 1.01–1.05), serum bicarbonate on day 1 (SHR 1.12, 95%CI 1.06–1.18), SOFA score (SHR 1.19, 95%CI 1.10–1.30), history of heart failure (SHR 3.71, 95%CI 1.63–8.46), and peak airway pressure (SHR 1.04, 95%CI 1.00–1.07). Stage III AKI was associated with a higher BMI (SHR 1.02, 95%CI 1.00–1.03), a history of DM (SHR 1.79, 95%CI 1.18–2.72), SOFA score (SHR 1.29, 95%CI 1.22–1.36), and arterial pH on day 1 (SHR per 0.1 units decrease was 1.25, 95%CI 1.05–1.49).

Conclusions

Age, a higher severity of illness, a history of diabetes, and acidosis were associated with development of AKI in ARDS patients. Severity of AKI was further associated with BMI, history of heart failure, and peak airway pressure.

Electronic supplementary material

The online version of this article (10.1186/s13613-019-0552-5) contains supplementary material, which is available to authorized users.

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Most cited references 31

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Effect of mechanical ventilation on inflammatory mediators in patients with acute respiratory distress syndrome: a randomized controlled trial.

V Ranieri, P Suter, C. Tortorella … (1999)

Studies have shown that an inflammatory response may be elicited by mechanical ventilation used for recruitment or derecruitment of collapsed lung units or to overdistend alveolar regions, and that a lung-protective strategy may reduce this response. To test the hypothesis that mechanical ventilation induces a pulmonary and systemic cytokine response that can be minimized by limiting recruitment or derecruitment and overdistention. Randomized controlled trial in the intensive care units of 2 European hospitals from November 1995 to February 1998, with a 28-day follow-up. Forty-four patients (mean [SD] age, 50 [18] years) with acute respiratory distress syndrome were enrolled, 7 of whom were withdrawn due to adverse events. After admission, volume-pressure curves were measured and bronchoalveolar lavage and blood samples were obtained. Patients were randomized to either the control group (n = 19): tidal volume to obtain normal values of arterial carbon dioxide tension (35-40 mm Hg) and positive end-expiratory pressure (PEEP) producing the greatest improvement in arterial oxygen saturation without worsening hemodynamics; or the lung-protective strategy group (n = 18): tidal volume and PEEP based on the volume-pressure curve. Measurements were repeated 24 to 30 and 36 to 40 hours after randomization. Pulmonary and systemic concentrations of inflammatory mediators approximately 36 hours after randomization. Physiological characteristics and cytokine concentrations were similar in both groups at randomization. There were significant differences (mean [SD]) between the control and lung-protective strategy groups in tidal volume (11.1 [1.3] vs 7.6 [1.1] mL/kg), end-inspiratory plateau pressures (31.0 [4.5] vs 24.6 [2.4] cm H2O), and PEEP (6.5 [1.7] vs 14.8 [2.7] cm H2O) (P<.001). Patients in the control group had an increase in bronchoalveolar lavage concentrations of interleukin (IL) 1beta, IL-6, and IL-1 receptor agonist and in both bronchoalveolar lavage and plasma concentrations of tumor necrosis factor (TNF) alpha, IL-6, and TNF-alpha, receptors over 36 hours (P<.05 for all). Patients in the lung-protective strategy group had a reduction in bronchoalveolar lavage concentrations of polymorphonuclear cells, TNF-alpha, IL-1beta, soluble TNF-alpha receptor 55, and IL-8, and in plasma and bronchoalveolar lavage concentrations of IL-6, soluble TNF-alpha receptor 75, and IL-1 receptor antagonist (P<.05). The concentration of the inflammatory mediators 36 hours after randomization was significantly lower in the lung-protective strategy group than in the control group (P<.05). Mechanical ventilation can induce a cytokine response that may be attenuated by a strategy to minimize overdistention and recruitment/derecruitment of the lung. Whether these physiological improvements are associated with improvements in clinical end points should be determined in future studies.

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The risk of acute renal failure in patients with chronic kidney disease.

C. -Y. Hsu, J D Ordoñez, G Chertow … (2008)

Few studies have defined how the risk of hospital-acquired acute renal failure varies with the level of estimated glomerular filtration rate (GFR). It is also not clear whether common factors such as diabetes mellitus, hypertension and proteinuria increase the risk of nosocomial acute renal failure independent of GFR. To determine this we compared 1,746 hospitalized adult members of Kaiser Permanente Northern California who developed dialysis-requiring acute renal failure with 600,820 hospitalized members who did not. Patient GFR was estimated from the most recent outpatient serum creatinine measurement prior to admission. The adjusted odds ratios were significantly and progressively elevated from 1.95 to 40.07 for stage 3 through stage 5 patients (not yet on maintenance dialysis) compared to patients with estimated GFR in the stage 1 and 2 range. Similar associations were seen after controlling for inpatient risk factors. Pre-admission baseline diabetes mellitus, diagnosed hypertension and known proteinuria were also independent risk factors for acute kidney failure. Our study shows that the propensity to develop in-hospital acute kidney failure is another complication of chronic kidney disease whose risk markedly increases even in the upper half of stage 3 estimated GFR. Several common risk factors for chronic kidney disease also increase the peril of nosocomial acute kidney failure.

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Fluid overload and mortality in children receiving continuous renal replacement therapy: the prospective pediatric continuous renal replacement therapy registry.

Douglas L Blowey, Michael Zappitelli, K D McBryde … (2010)

Critically ill children with hemodynamic instability and acute kidney injury often develop fluid overload. Continuous renal replacement therapy (CRRT) has emerged as a favored modality in the management of such children. This study investigated the association between fluid overload and mortality in children receiving CRRT. Prospective observational study. 297 children from 13 centers across the United States participating in the Prospective Pediatric CRRT Registry. Fluid overload from intensive care unit (ICU) admission to CRRT initiation, defined as a percentage equal to (fluid in [L] - fluid out [L])/(ICU admit weight [kg]) x 100%. The primary outcome was survival to pediatric ICU discharge. Data were collected regarding demographics, CRRT parameters, underlying disease process, and severity of illness. 153 patients (51.5%) developed or = 20% fluid overload. Patients who developed > or = 20% fluid overload at CRRT initiation had significantly higher mortality (61/93; 65.6%) than those who had 10%-20% fluid overload (22/51; 43.1%) and those with or = 20% and or = 20% fluid overload had an adjusted mortality OR of 8.5 (95% CI, 2.8-25.7). This was an observational study; interventions were not standardized. The relationship between fluid overload and mortality remains an association without definitive evidence of causality. Critically ill children who develop greater fluid overload before initiation of CRRT experience higher mortality than those with less fluid overload. Further goal-directed research is required to accurately define optimal fluid overload thresholds for initiation of CRRT. Copyright 2010 National Kidney Foundation, Inc. Published by Elsevier Inc. All rights reserved.

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Author and article information

Contributors

Anupol Panitchote: panupo@kku.ac.th

Omar Mehkri: mehkrio@ccf.org

Andrei Hasting: hastina@ccf.org

Tarik Hanane: hananet@ccf.org

Sevag Demirjian: demirjs@ccf.org

Heather Torbic: torbich@ccf.org

Eduardo Mireles-Cabodevila: mirelee@ccf.org

Sudhir Krishnan: krishns2@ccf.org

Abhijit Duggal: duggala2@ccf.org

Journal

Journal ID (nlm-ta): Ann Intensive Care

Journal ID (iso-abbrev): Ann Intensive Care

Title: Annals of Intensive Care

Publisher: Springer International Publishing (Cham )

ISSN (Electronic): 2110-5820

Publication date (Electronic): 1 July 2019

Publication date PMC-release: 1 July 2019

Publication date Collection: 2019

Volume: 9

Electronic Location Identifier: 74

Affiliations

[1 ]ISNI 0000 0001 0675 4725, GRID grid.239578.2, Department of Critical Care, Respiratory Institute, , Cleveland Clinic, ; Cleveland, OH USA

[2 ]ISNI 0000 0004 0470 0856, GRID grid.9786.0, Division of Critical Care Medicine, Department of Medicine, Faculty of Medicine, , Khon Kaen University, ; Khon Kaen, Thailand

[3 ]ISNI 0000 0001 0675 4725, GRID grid.239578.2, Department of Nephrology, , Cleveland Clinic, ; Cleveland, OH USA

[4 ]ISNI 0000 0001 0675 4725, GRID grid.239578.2, Department of Pharmacology, , Cleveland Clinic, ; Cleveland, OH USA

Article

Publisher ID: 552

DOI: 10.1186/s13613-019-0552-5

PMC ID: 6603088

PubMed ID: 31264042

SO-VID: a3973666-4ed4-48cf-a0c4-9f024b04bb88

License:

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.

History

Date received : 9 March 2019

Date accepted : 24 June 2019

Custom metadata

ScienceOpen disciplines: Emergency medicine & Trauma

Keywords: acute respiratory distress syndrome,acute kidney injury,mechanical ventilation,gas exchange,lung protective ventilation,septic shock

Data availability:

ScienceOpen disciplines: Emergency medicine & Trauma

Keywords: acute respiratory distress syndrome, acute kidney injury, mechanical ventilation, gas exchange, lung protective ventilation, septic shock

Factors associated with acute kidney injury in acute respiratory distress syndrome

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Abstract

Background

Methods

Results

Conclusions

Electronic supplementary material

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Karger: Nephrology

Most cited references 31

Effect of mechanical ventilation on inflammatory mediators in patients with acute respiratory distress syndrome: a randomized controlled trial.

The risk of acute renal failure in patients with chronic kidney disease.

Fluid overload and mortality in children receiving continuous renal replacement therapy: the prospective pediatric continuous renal replacement therapy registry.

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