Purpose: NT-proBNP, a peptide biomarker synthesized and secreted by cardiomyocytes in response to cardiac load, has gained attention in recent years for its potential role in respiratory diseases. Chronic Obstructive Pulmonary Disease (COPD), a chronic and progressive inflammatory condition affecting the respiratory system, is frequently associated with comorbidities involving the cardiovascular system. Consequently, the aim of this systematic review and meta-analysis was to evaluate the variations in NT-proBNP levels across distinct patient groups with COPD and establish a foundation for future investigations into the precise clinical significance of NT-proBNP in COPD. Methods: The search databases for this study were conducted in PubMed, Excerpt Medica database (Embase), Web of Science (WOS), and Cochrane Library databases. Databases were searched for studies on the predictive value of NT-proBNP in adult COPD patients. Results: A total of 29 studies (8534 participants) were included. Patients with stable COPD exhibit elevated levels of NT-proBNP [standardized mean difference(SMD) [95CI%]=0.51 [0.13,0.89]; p=0.0092]. COPD patients with predicted forced expiratory volume in 1 s (FEV₁) < 50% exhibit significantly elevated levels of NT-proBNP compared to those with FEV₁ ⩾50%[SMD [95CI%]=0.17 [0.05,0.29]; p=0.0058]. NT-proBNP levels were significantly higher in acute exacerbations (AECOPD) compared to patients with stable COPD [SMD [95CI%]=1.18 [0.07,2.29]; p=0.037]. NT-proBNP levels was significantly higher in non-survivors than in survivors of hospitalised AECOPD patients [SMD [95CI%]=1.67 [0.47,2.88]; p=0.0063]. Both COPD patients with pulmonary hypertension(PH) [SMD [95CI%]=0.82 [0.69,0.96]; p< 0.0001] and chronic heart failure(CHF) [SMD [95CI%]=1.49 [0.96,2.01]; p< 0.0001] showed higher NT-proBNP level. Conclusion: NT-proBNP, a biomarker commonly used in clinical practice to evaluate cardiovascular disease, demonstrates significant variations in different stages of COPD and during the progression of the disease. The fluctuations in NT-proBNP levels could be indicative of the severity of pulmonary hypoxia and inflammation and cardiovascular stress among COPD patients. Therefore, assessing NT-proBNP levels in COPD patients can aid in making informed clinical decisions.

Objective: To evaluate the clinical efficacy of high-flow nasal oxygen therapy (HFNC) and non-invasive ventilation (NIV) in patients with acute exacerbation of chronic obstructive pulmonary disease (AECOPD) after extubation. Research Methods: This systematic review and meta-analysis was conducted following the Preferred Reporting Items for Systematic Review and Meta-analyses (PRISMA) statements. The primary outcome measures analyzed included: reintubation rate, mortality, complication rate, and ICU length of stay. Results: Eight studies were included, with a total of 612 subjects, including 297 in the HFNC group and 315 in the NIV group. The effect of HFNC and NIV on the reintubation rate of AECOPD patients after extubation, RR (1.49 [95% CI,0.95 to 2.33], P = 0.082). Subgroup analysis with or without hypercapnia according to the included AECOPD population, with hypercapnia, RR (0.69 [95% CI,0.33 to 1.44], P=0.317), without hypercapnia, RR (2.61 [95% CI,1.41 to 4.83], P=0.002). Mortality, RR (0.92 [95% CI,0.56 to 1.52], P = 0.752). ICU length of stay, MD (− 0.44 [95% CI,-1.01 to 0.13], P = 0.132). Complication rate, RR (0.22 [95% CI,0.13 to 0.39], P = 0.000). After subgroup analysis, the reintubation rate of HFNC and NIV has no statistical difference in patients with hypercapnia, but NIV can significantly reduce the reintubation rate in patients without hypercapnia. In the outcome measures of complication rate, HFNC significantly reduced complication rate compared with NIV. In mortality and ICU length of stay, analysis results showed that HFNC and NIV were not statistically different. Conclusion: According to the available evidence, the application of HFNC can be used as an alternative treatment for NIV after extubation in AECOPD patients with hypercapnia, but in the patients without hypercapnia, HFNC is less effective than NIV.

Purpose: Omega-3 fatty acid is an emerging hotspot on anti-inflammation and chronic obstructive pulmonary disease (COPD) is known as a chronic inflammatory disease. The effect of Omega-3 fatty acid supplement on patients with COPD remains mixed for insufficient evidence. This systematic review and meta-analysis is based on neat randomized controlled trials trying to give a clearer impression on the effect of Omega-3 on patients with COPD. Methods: This systematic review and meta-analysis was conducted following the Preferred Reporting Items for Systematic Review and Meta-analyses (PRISMA) statements. Randomized clinical trials (RCTs) published in electronic databases including Medline, Embase, Cochrane Library, ClinicalTrials.gov and China National Knowledge Infrastructure (CNKI) by May 10, 2021 were searched. Data extracted from 6 predetermined domains (nutritional condition, lipid composition, inflammatory biomarker, lung function, physical endurance and quality of life [QoL]) were reviewed and analyzed. Results: A total of 8 RCTs evaluating 418 patients (age, mean [SD] = 67.3 [10.2] years) were included. Statistical differences were found in 3 parameters of 3 domains – weight (Wt) (0.25 [95% CI, 0.02 to 0.48], P = 0.03) in nutritional condition, low-density lipoprotein (LDL) (0.70 [95% CI, 0.30 to 1.10], P = 0.00) in lipid composition and interleukin-6 (IL-6) level (− 0.32 [95% CI, − 0.60 to − 0.05], P = 0.02) in inflammatory biomarker – while no significant difference was found in lung function, physical endurance or QoL. Conclusion: Comparing with placebo, Omega-3 intake was associated with more weight-gaining, LDL increase and IL-6 reduction. These results should be interpreted cautiously for the quality and quantity of available evidence are limited.

Diabetic kidney disease (DKD) is a major complication of diabetes mellitus, with its pathogenesis intricately regulated by dynamic feedback mechanisms. This comprehensive review systematically analyzes the hierarchical feedback networks driving DKD progression, spanning from systemic interactions to molecular cross-talks. We reveal that self-amplifying positive feedback loops dominate the disease process, manifested through three key dimensions: (1) The systemic triad of hyperglycemia-hypertension-proteinuria establishes a vicious cycle accelerating renal dysfunction; (2) Cellular homeostasis collapse through cross-amplified cell death modalities (apoptosis, pyroptosis, ferroptosis) and cell cycle dysregulation; (3) Molecular cascades centered on AGE/RAGE signaling that fuel chronic inflammation and fibrotic transformation. Collectively, these form a major positive feedback loop where PKC activation, oxidative stress propagation, and TGF-β-mediated fibrosis induced by hyperglycemia lead to progressive renal deterioration and fibrosis. Therapeutically, we propose a dual intervention strategy targeting both the acute phase through AGE/RAGE axis inhibition, coupled with chronic phase via precision modulation of fibrotic pathways. These findings redefine DKD progression as a self-reinforcing network disorder, providing a roadmap for developing multi-target therapies that disrupt pathological feedback loops while preserving renal repair mechanisms. Plain Language Summary: Positive feedback exists in diabetic kidney disease to drive disease progression.High glucose induced cell death and cell cycle disruption alter the cellular homeostasis.Fibrosis and inflammatory response, cell adhesion, angiogenesis, and thrombogenesis promote each other.The gradual development of the disease may lead to renal fibrosis and even end-stage renal disease.Diabetic kidney disease can be treated through intervention in the positive feedback process.