Backgroundsystemic inflammation disorders were observed in chronic kidney disease (CKD). Whether the systemic inflammatory indicators could be optimal predictors for the survival of CKD remains less studied.MethodsIn this study, participants were selected from the datasets of the National Health and Nutrition Examination Survey (NHANES) between 1999 to 2018 years. Four systemic inflammatory indicators were evaluated by the peripheral blood tests including systemic immune-inflammation index (SII, platelet*neutrophil/lymphocyte), neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), lymphocyte-to-monocyte ratio (LMR). Kaplan-Meier curves, restricted cubic spline (RCS), and Cox regression analysis were used to evaluate the association between the inflammatory index with the all-cause mortality of CKD. Receiver operating characteristic (ROC) and concordance index (C-index) were used to determine the predictive accuracy of varied systemic inflammatory indicators. Sensitive analyses were conducted to validate the robustness of the main findings.ResultsA total of 6,880 participants were included in this study. The mean age was 67.03 years old. Among the study population, the mean levels of systemic inflammatory indicators were 588.35 in SII, 2.45 in NLR, 133.85 in PLR, and 3.76 in LMR, respectively. The systemic inflammatory indicators of SII, NLR, and PLR were all significantly positively associated with the all-cause mortality of CKD patients, whereas the high value of LMR played a protectable role in CKD patients. NLR and LMR were the leading predictors in the survival of CKD patients [Hazard ratio (HR) =1.21, 95% confidence interval (CI): 1.07-1.36, p = 0.003 (3rd quartile), HR = 1.52, 95%CI: 1.35-1.72, p<0.001 (4th quartile) in NLR, and HR = 0.83, 95%CI: 0.75-0.92, p<0.001 (2nd quartile), HR = 0.73, 95%CI: 0.65-0.82, p<0.001 (3rd quartile), and = 0.74, 95%CI: 0.65-0.83, p<0.001 (4th quartile) in LMR], with a C-index of 0.612 and 0.624, respectively. The RCS curves showed non-linearity between systemic inflammatory indicators and all-cause mortality risk of the CKD population.ConclusionOur study highlights that systemic inflammatory indicators are important for predicting the survival of the U.S. population with CKD. The systemic inflammatory indicators would add additional clinical value to the health care of the CKD population.

目的:研究基于"心肾相关"的肾炎防衰液对糖尿病肾脏病(DKD)大鼠的治疗作用以及对肾脏及心脏病理的影响.方法:雄性SD大鼠40只,随机分出假手术组10只,余30只通过单侧肾结扎+链脲佐菌素(STZ)诱导成功建立DKD模型后,随机分为模型组、贝那普利组、肾炎防衰液组(n=10).治疗组分别予以贝那普利1.0 mg/kg·d-1、肾炎防衰液16.3 g/kg·d-1灌胃,余2组予以等量0.9％NaCl溶液.连续给药12周后,取血检测肌酐(Scr)、尿素氮(BUN)、血管紧张素Ⅱ(AngⅡ);用HE、PAS、Masson染色观察肾脏病理变化,HE、Masson染色观察心脏病理变化.结果:肾炎防衰液组和贝那普利组的Scr、BUN、AngⅡ水平相较于模型组均明显降低,差异均具有显著性(P<0.01,P<0.05).在肾脏病理中,与模型组相比,治疗组在HE、PAS、Mas-son染色中均体现出减轻肾病病理损害的作用;在心脏病理中,HE染色可见治疗组能减轻心脏病理损害,而Mas-son染色各组均未见明显纤维化组织.结论:基于心肾相关的肾炎防衰液能有效改善DKD大鼠肾功能,减轻其肾脏、心脏病理损害.

介绍徐书教授运用畅中攻下法治疗肾衰竭的经验.徐书教授认为肾衰的总病机是肾虚湿郁,湿浊是肾衰之标,脾肾不足、肝肾不足是本.本病因肾脏久病,或严重损伤引起脾肾阳虚,肝肾阴虚,日久又可因虚致实,本虚则清浊上逆,胃气不降;浊湿凝聚,郁阻中焦.两种病机都是本虚标实,徐书教授非常重视气机的升降,因此针对中焦气机受阻的多采用畅中攻下法以调畅中焦气机.

Background Chronic kidney disease (CKD) is one of the major causes of renal damage. Shenyan Fangshuai Recipe (SFR), a modified prescription of traditional medicine in China, showed potent effects in alleviating edema, proteinuria, and hematuria of CKD in clinical practices. In this study, we aimed to investigate scientific evidence-based efficacy as well as metabolic regulations of SFR in CKD treatment. Materials and Methods The effect of SFR on CKD was observed in a rat model which is established with oral administration of adenine-ethambutol mixture for 21 days. Further, metabolites in serum were detected and identified with ultra-performance liquid chromatography-high resolution mass spectrometry (UPLC-HRMS). Metabolomics study was performed using Ingenuity Pathway Analysis (IPA) software. Results With H&E staining and Masson's trichrome, the results showed that chronic kidney damage is significantly rescued with SFR treatment and recovered to an approximately normal condition. Along with 44 differential metabolites discovered, the regulation of SFR on CKD was enriched in glycine biosynthesis I, mitochondrial L-carnitine shuttle pathway, phosphatidylethanolamine biosynthesis III, sphingosine-1-phosphate signaling, L-serine degradation, folate transformations I, noradrenaline and adrenaline degradation, salvage pathways of pyrimidine ribonucleotides, cysteine biosynthesis III (Mammalia), glycine betaine degradation, and cysteine biosynthesis/homocysteine degradation. Further, TGFβ-1 and MMP-9 were observed playing roles in this regulatory process by performing immunohistochemical staining. Conclusion SFR exerts potent effects of alleviating glomerular sclerosis and interstitial fibrosis in the kidney, mainly via integrated regulations on metabolism and production of homocysteine, L-carnitine, and epinephrine, as well as the expression of TGFβ-1. This study provides evidence for SFR's protective effects on CKD and reveals the metabolic mechanism behind these benefits for the first time.

Chronic pain is a major health problem, which can impair quality of life and reduce productivity. Electroacupuncture (EA), a modality of medicine based on the theories of Traditional Chinese Medicine (TCM), presents great therapeutic effects on chronic pain. Its clinical application has gained increasing popularity, and in parallel, more research has been performed on the mechanisms of EA-induced analgesia. The past decades have seen enormous advances both in neuronal circuitry of needle-insertion and in its molecular mechanism. EA may block pain by activating the descending pain inhibitory system, which originates in the brainstem and terminates at the spinal cord. This review article synthesizes corresponding studies to elucidate how EA alleviate pain via the mediation of this descending system. Much emphasis has been put on the implication of descending serotonergic and noradrenergic pathways in the process of pain modulation. Also, other important transmitters and supraspinal regions related to analgesic effects of EA have been demonstrated. Finally, it should be noticed that there exist some shortcomings involved in the animal experimental designed for EA, which account for conflicting results obtained by different studies.