PURPOSE: The soluble form of the receptor for advanced glycation end-products (sRAGE) is a promising marker for epithelial dysfunction, but it has not been fully characterized as a biomarker of acute respiratory distress syndrome (ARDS). Whether sRAGE could inform on the response to ventilator settings has been poorly investigated, and whether a recruitment maneuver (RM) may influence plasma sRAGE remains unknown. METHODS:Twenty-four patients with moderate/severe, nonfocal ARDS were enrolled in this prospective monocentric crossover study and randomized into a "RM-SHAM" group when a 6-h-long RM sequence preceded a 6-h-long sham evaluation period, or a "SHAM-RM" group (inverted sequences). Protective ventilation was applied, and RM consisted of the application of 40 cmH2O airway pressure for 40 s. Arterial blood was sampled for gas analyses and sRAGE measurements, 5 min pre-RM (or 40-s-long sham period), 5, 30 min, 1, 4, and 6 h after the RM (or 40-s-long sham period). RESULTS:Mean PaO2/FiO2, tidal volume, PEEP, and plateau pressure were 125 mmHg, 6.8 ml/kg (ideal body weight), and 13 and 26 cmH2O, respectively. Median baseline plasma sRAGE levels were 3,232 pg/ml. RM induced a significant decrease in sRAGE (-1,598 ± 859 pg/ml) in 1 h (p = 0.043). At 4 and 6 h post-RM, sRAGE levels increased back toward baseline values. Pre-RM sRAGE was associated with RM-induced oxygenation improvement (AUC 0.84). CONCLUSIONS: We report the first kinetics study of plasma sRAGE after RM in ARDS. Our findings reinforce the value of plasma sRAGE as a biomarker of ARDS.
RCT Entities:
PURPOSE: The soluble form of the receptor for advanced glycation end-products (sRAGE) is a promising marker for epithelial dysfunction, but it has not been fully characterized as a biomarker of acute respiratory distress syndrome (ARDS). Whether sRAGE could inform on the response to ventilator settings has been poorly investigated, and whether a recruitment maneuver (RM) may influence plasma sRAGE remains unknown. METHODS: Twenty-four patients with moderate/severe, nonfocal ARDS were enrolled in this prospective monocentric crossover study and randomized into a "RM-SHAM" group when a 6-h-long RM sequence preceded a 6-h-long sham evaluation period, or a "SHAM-RM" group (inverted sequences). Protective ventilation was applied, and RM consisted of the application of 40 cmH2O airway pressure for 40 s. Arterial blood was sampled for gas analyses and sRAGE measurements, 5 min pre-RM (or 40-s-long sham period), 5, 30 min, 1, 4, and 6 h after the RM (or 40-s-long sham period). RESULTS: Mean PaO2/FiO2, tidal volume, PEEP, and plateau pressure were 125 mmHg, 6.8 ml/kg (ideal body weight), and 13 and 26 cmH2O, respectively. Median baseline plasma sRAGE levels were 3,232 pg/ml. RM induced a significant decrease in sRAGE (-1,598 ± 859 pg/ml) in 1 h (p = 0.043). At 4 and 6 h post-RM, sRAGE levels increased back toward baseline values. Pre-RM sRAGE was associated with RM-induced oxygenation improvement (AUC 0.84). CONCLUSIONS: We report the first kinetics study of plasma sRAGE after RM in ARDS. Our findings reinforce the value of plasma sRAGE as a biomarker of ARDS.
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