Soluble Receptor for Advanced Glycation End-Products Predicts Impaired Alveolar Fluid Clearance in Acute Respiratory Distress Syndrome

Jabaudon, Matthieu; Blondonnet, Raïko; Roszyk, Laurence; Bouvier, Damien; Audard, Jules; Clairefond, Gaël; Fournier, Mathilde; Marceau, Geoffroy; Déchelotte, P.; Pereira, Bruno; Sapin, Vincent; Constantin, Jean-Michel

doi:10.1164/rccm.201501-0020oc

Cited by 133 publications

(151 citation statements)

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“…Thus, it seems reasonable to supplement increasing ARDS awareness with biomarkers of acute lung damage like SPD and probably others. In a rat model of ARDS, soluble receptor for advanced glycation end products (sRAGE) seemed to reflect alveolar type I cell injury, and this was also observed in humans [29, 30], and recently, it has been demonstrated that a strong negative correlation exists between alveolar fluid clearance rate and plasma sRAGE in a murine model as well as in humans [31]. Thus, sRAGE and SPD may provide complementary information on the pathophysiological changes taking place in the alveolar epithelium.…”

Section: Discussionmentioning

confidence: 99%

Prediction of non-recovery from ventilator-demanding acute respiratory failure, ARDS and death using lung damage biomarkers: data from a 1200-patient critical care randomized trial

Itenov

Þormar

Hein

et al. 2016

Ann. Intensive Care

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BackgroundIt is unclear whether biomarkers of alveolar damage (surfactant protein D, SPD) or conductive airway damage (club cell secretory protein 16, CC16) measured early after intensive care admittance are associated with one-month clinical respiratory prognosis. If patients who do not recover respiratory function within one month can be identified early, future experimental lung interventions can be aimed toward this high-risk group. We aimed to determine, in a heterogenous critically ill population, whether baseline profound alveolar damage or conductive airway damage has clinical respiratory impact one month after intensive care admittance.MethodsBiobank study of biomarkers of alveolar and conductive airway damage in intensive care patients was conducted. This was a sub-study of 758 intubated patients from a 1200-patient randomized trial. We split the cohort into a “learning cohort” and “validating cohort” based on geographical criteria: northern sites (learning) and southern sites (validating).ResultsBaseline SPD above the 85th percentile in the “learning cohort” predicted low chance of successful weaning from ventilator within 28 days (adjusted hazard ratio 0.6 [95% CI 0.4–0.9], p = 0.005); this was confirmed in the validating cohort. CC16 did not predict the endpoint. The absolute risk of not being successfully weaned within the first month was 48/106 (45.3%) vs. 175/652 (26.8%), p < 0.0001 (high SPD vs. low SPD). The chance of being “alive and without ventilator ≥20 days within the first month” was lower among patients with high SPD (adjusted OR 0.2 [95% CI 0.2–0.4], p < 0.0001), confirmed in the validating cohort, and the risk of ARDS was higher among patients with high SPD (adjusted OR 3.4 [95% CI 1.0–11.4], p = 0.04)—also confirmed in the validating cohort.ConclusionEarly profound alveolar damage in intubated patients can be identified by SPD blood measurement at intensive care admission, and high SPD level is a strong independent predictor that the patient suffers from ARDS and will not recover independent respiratory function within one month. This knowledge can be used to improve diagnostic and prognostic models and to identify the patients who most likely will benefit from experimental interventions aiming to preserve alveolar tissue and therefore respiratory function. Trial registration This is a sub-study to the Procalcitonin And Survival Study (PASS), Clinicaltrials.gov ID: NCT00271752, first registered January 1, 2006Electronic supplementary materialThe online version of this article (doi:10.1186/s13613-016-0212-y) contains supplementary material, which is available to authorized users.

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Section: Discussionmentioning

confidence: 99%

Prediction of non-recovery from ventilator-demanding acute respiratory failure, ARDS and death using lung damage biomarkers: data from a 1200-patient critical care randomized trial

Itenov

Þormar

Hein

et al. 2016

Ann. Intensive Care

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“…As the ALI/ARDS resolves in patients, plasma sRAGE levels also fall, suggesting that sRAGE can act not only as a marker of disease severity and prognosis but also as a marker of resolving disease [99,100]. …”

Section: Rage In Pulmonary Diseasesmentioning

confidence: 99%

All the “RAGE” in lung disease: The receptor for advanced glycation endproducts (RAGE) is a major mediator of pulmonary inflammatory responses

Oczypok

Perkins

Oury

2017

Paediatric Respiratory Reviews

169

194

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SUMMARY The receptor for advanced glycation endproducts (RAGE) is a pro-inflammatory pattern recognition receptor (PRR) that has been implicated in the pathogenesis of numerous inflammatory diseases. It was discovered in 1992 on endothelial cells and was named for its ability to bind advanced glycation endproducts and promote vascular inflammation in the vessels of patients with diabetes. Further studies revealed that RAGE is most highly expressed in lung tissue and spurred numerous explorations into RAGE’s role in the lung. These studies have found that RAGE is an important mediator in allergic airway inflammation (AAI) and asthma, pulmonary fibrosis, lung cancer, chronic obstructive pulmonary disease (COPD), acute lung injury, pneumonia, cystic fibrosis, and bronchopulmonary dysplasia. RAGE has not yet been targeted in the lungs of paediatric or adult clinical populations, but the development of new ways to inhibit RAGE is setting the stage for the emergence of novel therapeutic agents for patients suffering from these pulmonary conditions.

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“…Small RCTs have shown that IOLPV causes an attenuated release of local and systemic inflammatory mediators after cardiopulmonary bypass, major abdominal surgery, and esophagectomy 198687. In open abdominal surgery, investigators have shown improvements in both intraoperative and postoperative pulmonary mechanics.…”

Section: Evidence Based Strategies For Perioperative Lung Protective mentioning

confidence: 99%

Perioperative lung protective ventilation

O’Gara

Talmor

2018

BMJ

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Perioperative lung injury is a major source of postoperative morbidity, excess healthcare use, and avoidable mortality. Many potential inciting factors can lead to this condition, including intraoperative ventilator induced lung injury. Questions exist as to whether protective ventilation strategies used in the intensive care unit for patients with acute respiratory distress syndrome are equally beneficial for surgical patients, most of whom do not present with any pre-existing lung pathology. Studied both individually and in combination as a package of intraoperative lung protective ventilation, the use of low tidal volumes, moderate positive end expiratory pressure, and recruitment maneuvers have been shown to improve oxygenation and pulmonary physiology and to reduce postoperative pulmonary complications in at risk patient groups. Further work is needed to define the potential contributions of alternative ventilator strategies, limiting excessive intraoperative oxygen supplementation, use of non-invasive techniques in the postoperative period, and personalized mechanical ventilation. Although the weight of evidence strongly suggests a role for lung protective ventilation in moderate risk patient groups, definitive evidence of its benefit for the general surgical population does not exist. However, given the shift in understanding of what is needed for adequate oxygenation and ventilation under anesthesia, the largely historical arguments against the use of intraoperative lung protective ventilation may soon be outdated, on the basis of its expanding track record of safety and efficacy in multiple settings.

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Soluble Receptor for Advanced Glycation End-Products Predicts Impaired Alveolar Fluid Clearance in Acute Respiratory Distress Syndrome

Cited by 133 publications

References 46 publications

Prediction of non-recovery from ventilator-demanding acute respiratory failure, ARDS and death using lung damage biomarkers: data from a 1200-patient critical care randomized trial

Prediction of non-recovery from ventilator-demanding acute respiratory failure, ARDS and death using lung damage biomarkers: data from a 1200-patient critical care randomized trial

All the “RAGE” in lung disease: The receptor for advanced glycation endproducts (RAGE) is a major mediator of pulmonary inflammatory responses

Perioperative lung protective ventilation

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