Stable angina pectoris is experienced as trans-sternal or retro-sternal pressure or pain that may radiate to the left arm, neck or back. Although available evidence relating to its effectiveness and mechanism are weak, traditional Chinese medicine is used as an alternative therapy for stable angina pectoris. We report a protocol of a randomized controlled trial using traditional Chinese medicine to investigate the effectiveness, mechanism and safety for patients with stable angina pectoris. This is a north-east Chinese, multi-center, multi-blinded, placebo-controlled and superiority randomized trail. A total of 240 patients with stable angina pectoris will be randomly assigned to three groups: two treatment groups and a control group. The treatment groups will receive Chinese herbal medicine consisting of Yi-Qi-Jian-Pi and Qu-Tan-Hua-Zhuo granule and Yi-Qi-Jian-Pi and Qu-Tan-Hua-Yu granule, respectively, and conventional medicine. The control group will receive placebo medicine in addition to conventional medicine. All 3 groups will undergo a 12-week treatment and 2-week follow-up. Four visits in sum will be scheduled for each subject: 1 visit each in week 0, week 4, week 12 and week 14. The primary outcomes include: the frequency of angina pectoris attack; the dosage of nitroglycerin; body limited dimension of Seattle Angina Questionnaire. The secondary outcomes include: except for the body limited dimension of SAQ, traditional Chinese medicine pattern questionnaire and so on. Therapeutic mechanism outcomes, safety outcomes and endpoint outcomes will be also assessed. The primary aim of this trial is to develop a standard protocol to utilize high-quality EBM evidence for assessing the effectiveness and safety of SAP via TCM pattern differentiation as well as exploring the efficacy mechanism and regulation with the molecular biology and systems biology. Clinical Trials Registration: ChiCTR-TRC-13003608 , registered 18 June 2013.

Chronic kidney disease (CKD) and cardiovascular disease are bidirectionally linked, with metabolic reprogramming as a central pathophysiological nexus. This review examines metabolic disturbances underlying CKD–CVD comorbidity, including energy metabolism disorders, mitochondrial dysfunction, lipid and glucose dysregulation, and mineral metabolism abnormalities. The gut microbiota–metabolic axis contributes through depletion of short-chain fatty acids, accumulation of trimethylamine N-oxide, and production of uremic toxins. These changes compromise intestinal barrier integrity and sustain systemic inflammation. Downstream consequences include oxidative stress, NLRP3 inflammasome activation, cardiac and renal fibrosis, vascular calcification, and endothelial dysfunction. We critically distinguish validated interventions from speculative strategies. SGLT2 inhibitors and GLP-1 receptor agonists have established cardiorenal protection in large randomized trials, with effects extending beyond glycemic control. By contrast, gut microbiota modulation, mitochondria-targeted therapies, and several anti-inflammatory and anti-fibrotic strategies remain at the preclinical or early-phase clinical stage, and a number of mechanistically attractive interventions have failed in confirmatory trials. We also outline areas of contradictory evidence and unresolved questions. Future directions include multi-omics integration, metabolic phenotype-based stratification, and rational drug development targeting central metabolic nodes. The review provides mechanistic insights into metabolic–immune–inflammatory crosstalk in CKD–CVD and highlights priorities for translation.