Acute kidney injury (AKI) is a major renal disease associated with a high mortality rate and increasing prevalence. Decades of research has suggested numerous chemical and biological agents with beneficial effects in AKI. In addition, cell therapy and molecular targeting have been explored for reducing kidney tissue damage and promoting kidney repair or recovery from AKI. Mechanistically, these approaches may mitigate oxidative stress, inflammation, cell death, and mitochondrial and other organellar damage, or activate cytoprotective mechanisms such as autophagy and pro-survival factors. However, none of these findings has been successfully translated into clinical treatment of AKI. In this review, we analyze these findings and propose experimental strategies for the identification of renoprotective agents or methods with clinical potential. Moreover, we propose the consideration of combination therapy by targeting multiple targets in AKI.

Chronic cough due to non-acid reflux may be related to cough reflex hypersensitivity caused by neurogenic airway inflammation and mast cell activation, in which weakly acidic reflux is possibly a major factor.

BackgroundCigarette smoking is the most commonly encountered and readily identifiable risk factor for COPD. However, it is not clear which quantitative factors related to smoking influence the prognosis of COPD patients.MethodsA total of 204 patients with a long-term history of smoking were enrolled into this study and followed up for 5 years. Patients were divided into “death” or “survival” groups based on follow-up results and “quitting-smoking” or “continuing-smoking” groups based on whether they gave up smoking.ResultsPatients in the death group had a longer smoking time, lower prevalence of quitting smoking, later onset of COPD symptoms, older age at quitting smoking, lower forced expiratory volume in one second (FEV1) % predicted, and lower ratio of FEV1/forced vital capacity. Age, age at quitting smoking, and FEV1% predicted were independently associated with mortality from COPD. Compared to the continuing-smoking group, the quitting-smoking group had a lower mortality rate, longer course of COPD, earlier onset of COPD symptoms, and lower residual volume percent predicted. During the 5-year follow-up, 113 deaths were recorded (quitting-smoking group: n=92; 40 deaths; continuing-smoking group: n=112; 73 deaths). The mortality risk remained significantly higher in the continuing-smoking group than the quitting-smoking group (log-rank test, 13.59; P=0.0002).ConclusionSmoking time may be related to the mortality rate from COPD. Smoking cessation has the greatest capacity to influence the natural history of COPD.

Background: The frequency distributions of the etiologies of chronic cough have changed over time. This study aimed to investigate the changing etiological frequency of chronic cough in a tertiary hospital in Shanghai, China, and to explore the clinical significance. Methods: Medical records of 1,311 patients with chronic cough who visit our hospital between January 2009 and December 2016 were retrospectively reviewed. The etiologies of chronic cough were identified according to a standardized step-by-step diagnostic protocol and the changes in the etiological frequency of chronic cough over the years were using the Chi-squared (ꭓ 2) test. Results: Cough variant asthma (CVA) (449/1,311, 34.2%), gastroesophageal reflux-related chronic cough (GERC) (374/1,311, 28.5%), upper airway cough syndrome/postnasal drip syndrome (UACS/PNDs) (241/1,311, 18.4%), atopic cough (AC) (188/1,311, 14.3%), and non-asthmatic eosinophilic bronchitis (NAEB) (147/1,311, 11.2%) were the common causes of chronic cough in descending order. The postinfectious cough (PIC) (39/1,311, 3.0%) and angiotensin-converting enzyme inhibitor (ACEI)-induced cough (25/1,311, 1.9%) were less common. During the 8-year period, the proportion of CVA (ꭓ 2 =72.86, P<0.0001) and UACS/PNDs (ꭓ 2 =68.80, P<0.0001) decreased, while those of NAEB (ꭓ 2 =51.38, P<0.0001), GERC (ꭓ 2 =55.95, P<0.0001) and AC (ꭓ 2 =39.09, P<0.0001) increased. Conclusions: The etiological frequency of chronic cough varies over time, and it may encourage the adjustment of the current diagnostic and therapeutic strategies for chronic cough.

Three-step empirical therapy seemed to be useful in most patients and has practical application in the management of chronic cough.