Circulating angiotensin peptides levels in Acute Respiratory Distress Syndrome correlate with clinical outcomes: A pilot study

Abstract

Rationale We propose renin angiotensin system (RAS) peptides are critical in wound reparative processes such as in acute respiratory distress syndrome (ARDS). Their role in predicting clinical outcomes in ARDS has been unexplored; thus, we used a targeted metabolomics approach to investigate them as potential predictors of outcomes. Methods Thirty-nine ARDS patients were enrolled within 24 hours of ARDS diagnosis. Plasma RAS peptide levels were quantified at study entry and 24, 48 and 72 hours using a liquid chromatography-mass spectrometry based metabolomics assay. RAS peptide concentrations were compared between survivors and non-survivors, and were correlated with clinical and pulmonary measures. Measurements and main results Angiotensin I (Ang-I or A(1–10)) levels were significantly higher in non-survivors at study entry and 72 hours. ARDS survival was associated with lower A(1–10) concentration (OR 0.36, 95% CI 0.18–0.72, p = 0.004) but higher A(1–9) concentration (OR 2.24, 95% CI 1.15–4.39, p = 0.018), a biologically active metabolite of A(1–10) and an agonist of angiotensin II receptor type 2. Survivors had significantly higher median A(1–9)/A(1–10) and A(1–7)/A(1–10) ratios than the non-survivors (p = 0.001). Increased A(1–9)/A(1–10) ratio suggests that angiotensin converting enzyme II (ACE2) activity is higher in patients who survived their ARDS insult while an increase in A(1–7)/A(1–10) ratio suggests that ACE activity is also higher in survivors. Conclusion A(1–10) accumulation and reduced A(1–9) concentration in the non-survivor group suggest that ACE2 activities may be reduced in patients succumbing to ARDS. Plasma levels of both A(1–10) and A(1–9) and their ratio may serve as useful biomarkers for prognosis in ARDS patients.

Prognostic Value of N-terminal Probrain Natriuretic Peptide for Patients with Acute Respiratory Distress Syndrome: A Systematic Review and Meta-Analysis

“…Not relevant:30 Animal study: 1 Non-adult studies:2 Figure 1: Flow diagram of the study selection process. 4 BioMed Research International were found in the subgroup analysis of the summary specificity (P > 0:05) ( Table 3).…”

“…Early prediction of poor prognosis in ARDS patients after intensive care unit (ICU) admission would enable physicians to implement more effective treatment strategies to improve survival. Previous studies have shown that several biomarkers such as plasma angiotensin peptides and interleukin-18 are associated with the prognosis of ARDS patients [4,5], but these biomarkers are not widely used in clinical applications. Therefore, it is crucial to identify a reliable biomarker that can predict the prognosis of these patients in a clinical setting.…”

Angiotensin I and angiotensin II concentrations and their ratio in catecholamine-resistant vasodilatory shock

“…To our knowledge, this is one of the first studies to evaluate serum ANG I and ANG II levels and the ANG I/II ratio in patients with CRVS. Only a single recent pilot study found that increased ANG I levels were correlated with mortality [29]. In comparison, our study was much larger and involved several hundred patients in multiple countries and continents, thus providing a high level of external validity.…”

Are Losartan and Imatinib Effective Against SARS-CoV2 Pathogenesis? a Pathophysiologic-Based in Silico Study

“…33,34 Angiotensin [1][2][3][4][5][6][7] is considered as an active peptide in RAS with antioxidative, anti-inflammatory, antiproliferative/antifibrotic, potent vasodilatory, and anti-thrombotic properties which exerts most of its effect via Mas receptor. 34,35,36,37 On the other side of this intricate-regulatory RAS, ACE increases Ang II with its oxidative, proinflammatory, proliferative/fibrotic, vasoconstrictive and thrombotic effects which is mostly exerted through angiotensin II type 1 receptor (AT1R). Another receptor for Ang II called angiotensin II type 2 receptor (AT2R) with cell protective and some opposing post-receptor effects to AT1R is distribute in a limited number of organs.…”