Acute kidney injury in hospitalized patients with nonexacerbated chronic obstructive pulmonary disease.

BACKGROUND: The epidemiology of acute kidney injury (AKI) in nonexacerbated chronic obstructive pulmonary disease (NECOPD) patients is unknown. This study investigated the factors associated with AKI and the association between AKI and in-hospital mortality in the hospitalized NECOPD population. METHODS: The electronic medical records of 2897 patients hospitalized with NECOPD were analyzed retrospectively. Demographic information, medicine used before AKI, diagnosis records and laboratory data were collected. AKI was classified as community-acquired (CA-) or hospital-acquired (HA-) AKI according to the serum creatinine criteria. Risk factors for HA-AKI and in-hospital mortality were analyzed by logistic regression analyses. To avoid an interaction between cor pulmonale and AKI, the association between AKI and in-hospital morality was further analyzed with cor pulmonale stratification. RESULTS: The incidence rates of CA- and HA-AKI were 7.1 and 12.0%, respectively. Increased age, female sex, cor pulmonale comorbidity, chronic kidney disease stage, diuretic and glycopeptide use before AKI and iodine-containing contrast medium exposure were independently associated with HA-AKI. A total of 5.7% of the patients died. After adjustment for age, sex, cor pulmonale, chronic kidney disease, Charlson comorbidity index score (without renal disease) and hemoglobin level, HA-AKI was an independent risk factor for in-hospital mortality [OR 13.909 (95% CI 8.699-22.238) in non-cor pulmonale subgroup; OR 26.604 (95% CI 12.166-58.176) in cor pulmonale subgroup], whereas CA-AKI was not. CONCLUSIONS: AKI is common in the NECOPD population. Diuretics and contrast media are associated with HA-AKI in this population. The patients with HA-AKI have a higher mortality risk than the patients without AKI.

Serum Endostatin Is a Novel Marker for COPD Associated with Lower Lung Function, Exacerbation and Systemic Inflammation.

Backgrounds and Aims: It is well known that angiogenesis contributes to the progression of chronic obstructive pulmonary disease (COPD) by initiating the remodeling of bronchial vasculature. However, the specific molecular mechanisms are incompletely understood. This research aimed to explore whether endostatin, a member of endogenous antiangiogenic proteins, is a biomarker in COPD and plays a role in the angiogenesis of COPD. Methods: 100 stable COPD patients, 130 patients with acute exacerbation (AECOPD) and 68 healthy volunteers were recruited in this research. Lung function test was conducted in the healthy people and stable COPD patients. Serum endostatin, C-reactive protein (CRP) and vascular endothelial growth factor (VEGF) of all the subjects were measured by Human Magnetic Luminex Screening Assay. Results: Serum endostatin level was significantly higher in stable COPD compared with healthy control and even more in AECOPD patients (P<0.001). Besides, stable COPD patients with frequent exacerbation (≥2 exacerbations per year) in the last 1 year had a higher concentration of endostatin in the circulation compared to the patients with less exacerbation (P=0.037). Furthermore, circulatory endostatin was negatively associated with forced expiratory volume in 1 s % predicted (FEV1%pre), an index of lung function in the stable COPD group (P=0.009). Finally, endostatin was positively correlated to serum CRP in COPD group (including stable and AECOPD) (P=0.005) and all the subjects (P<0.001), but only associated with VEGF in the total participants (P=0.002), not in the COPD group. Conclusion: These results suggested that endostatin is a biomarker for COPD and associated with lower lung function, exacerbation, and systemic inflammation. Endostatin potentially contributes to the pathogenesis of COPD.

Circulating syndecan-1 as a novel biomarker relates to lung function, systemic inflammation, and exacerbation in COPD.

Introduction: Patients with COPD often show increased systemic inflammation which is associated with lower functional status, greater exacerbation risk, and worse clinical outcomes. Syndecans (SDCs), a family of transmembrane heparan sulfate proteoglycans (HSPGs), have been found to involve in inflammatory processes in many chronic inflammatory diseases. The aim of this preliminary clinical study was to investigate the possible association between two SDCs, SDC-1 and SDC-4, with lung function, systemic inflammation, and risk of exacerbations in COPD patients. Method: Serum SDC-1 and SDC-4 levels were measured in 101 COPD patients and 57 health controls. Correlations between SDCs and other parameters were analyzed using Spearsman's rho. Receiver operating curve (ROC) analysis was used to evaluate the threshold value in differentiating disease status. Results: Although both serum SDC-1 and SDC-4 showed a downward trend in COPD patients, only SDC-1 levels were correlated positively with the ratio of FEV1/FVC and parameters of small airway obstruction. Besides, SDC-1 but not SDC-4, was negatively correlated with C-reactive protein (CRP) in COPD patients and downregulated in frequent exacerbators (FEs) of COPD. Using a cutoff value of 2.08 ng/mL, the sensitivity and specificity of SDC-1 to differentiate FE were 44% and 93.4%, respectively. Conclusion: In conclusion, circulating SDC-1 may be a novel inflammatory biomarker associated with lung function and systemic inflammation in patients with COPD, which could also be useful to identify the risk of COPD exacerbation. Further studies should be performed to clarify the influences of SDC-1 on the pathogenesis and outcomes of COPD.