Introduction: To investigate whether tripotolide have direct effect on podocytes injured by AngII ? If so, how does it work?Methodology: Conditionally immortalized mouse podocytes were divided into three groups: negative control, positive control treated with AngII (10^-6, 10^-7, 10^-8mol/L) and pretreated with triptolide (1, 3, 10ng/ml) for 2 hours. F-actin and zonula occludens-1 (ZO-1) were observed by fluorescence microscopy. To explore the underlying mechanism，we observed reactive oxygen species (ROS) generation and the subsequent MAPK activation by flow cytometry and western blot.Results: Ang II induced actin cytoskeleton reorganization and ZO-1 redistribution in a dose-dependent manner. In untreated podocytes, the ZO-1 staining was peripherally distributed at contacts of adjacent cells as fine segments, while it appeared markedly fragmented in response Ang II, indicating tight junction loose and cell ruffling. Triptolide stabilized actin filaments and improved ZO-1 distribution in a dose dependent manner. At the dose of 10ng/ml, triptolide almost completely restored the normal cytoskeleton and cell contact in podocytes without affecting cell survival. AngII (10^-7mol/L) significantly increased ROS generation in podocytes. This effect was observed rapidly at 10min and maintained for 30min. Pretreatment of podocytes with triptolide (10ng/ml) or antioxidant NAC (10 mmol/L) before AngII exposure led to a significant reduction in the cellular ROS level. In addition, antioxidant NAC successfully reduced AngII-induced podocyte damage as showed by cytoskeleton staining, indicating that ROS generation mediates Ang-induced podocyte injury. Furthermore, triptolide effectively inhibited AngII-induced p38, ERK1/2 and JNK MAPK activation, which are the downstream signaling molecules of ROS. SB203580 and U0126, which are specific kinase inhibitor for p-38 and ERK MAPK, can block AngII induced podocyte injury.Conclusion: Triptolide showed dramatic protective effect in AngII induced podocyte injury. The protective effect of triptolide might partially due to the inhibition of ROS generation and the subsequent MAPK activation.

Systemic lupus erythematosus (SLE) is an autoimmune disease with complex pathogenesis and diverse clinical manifestations. In recent years, as theoretical and technological innovations in the postgenomic era, specifically advances in gene detection techniques, over 30 diseasecausing genes for SLE have been identified and the concept of “Monogenic lupus” has been proposed. This review will focus on the pathogenesis, clinical manifestations and genetic diagnosis of these genes, so as to raise awareness of the genetic contribution to SLE and advance further research.

Acute kidney injury (AKI)has a rapid onset, but there is no early and sensitive indicator for dynamic monitoring of kidney function. Studies have found ferroptosis occured in various AKI models, and specific proteins and genes involved in ferroptosis are expected to be predictors of the occurrence and development of AKI. Ferroptosis is closely related to the metabolism of iron, amino acids and lipids, and it participates in development of AKI through pathological processes such as inflammation, endoplasmic reticulum stress and autophagy. Studies have confirmed that many kinds of drugs targeting on ferroptosis have achieved good efficacy in the treatment of AKI. This article reviews the mechanism of ferroptosis involved in development of AKI and the latest research progress of drugs for treatment of ferroptosis.

Systemic light chain (AL) amyloidosis is a rare plasma cell disease that often causes dysfunction of important organs such as heart and kidney. In recent years, some progress has been made in the field of molecular mechanism of AL amyloidosis, which helps us further understand structural characteristics of amyloid fibrils in AL amyloidosis and pathological mechanism of heart and kidney damage; In addition, there has been some advances in diagnosis and treatment of AL amyloidosis, which is of great significance for improving clinical practice of AL amyloidosis. This article will review recent progress in pathogenesis, diagnosis and treatment of AL amyloidosis.

【Abstract】 In the kidney, microvascular pericytes are extensively branched, collagen-producing cells in close contact with endothelial cells. These cells contribute to the stability of microvascular in physiological condition. After continuous renal injury, the pericytes detach from the basement of capillaries and transform to scar-forming myofibroblasts. Inhibit pericyte-myofibroblasts transforming improve the renal fibrosis and peritubular capillary rarefaction. Additionally, the pericyte may be the major erythropoietin-producing cell in the kidney. In the patients of chronic kidney disease, transforming to myofibroblast make the pericyte effectiveless in producing the erythropoietin although the marked anemia. The research about the pericyte in kidney has made great process in recent years. Learning about the function of pericyte help us to understand the mechanism of renal fibrosis. Furthermore, the therapy targeting the pericyte may be helpful in preventing the progress of renal fibrosis.

Diabetes mellitus is a group of metabolic diseases characteized by hyperghycemia.With the economic development and lifestyle changes,the prevalence of diabetes has gradually increased,and it has become an increasingly serious public health problem in most regions of the world.Presenting a heterogeneous etiology,the pathogenic mechanisms of diabetes is still unclear and effective therapeutic methods need to be explored.Studies in animal models are contributing to  understanding of the pathogenic mechanism of diabetes and development of drugs.Zebrafish is superior to other model systems,rapidly emerging as promising model organism for functional studies of human disease，including inducedproximity models and genetically modified models with spontaneous diabetes.This article reviews the progresses of current researches using diabetic zebrafish models.

This article introduces 4 national standards for the infrastructure construction and operation management of the biobank, GB／T 39766-2021Management specification for human biobank, GB／T 39767-2021 Management specification for human biomaterial, GB／T40364-2021 Fundamental terminology for human biobank and GB／T 39768-2021 Classification and coding for human biomaterial.We systematically describe the standardized organizational structure, personnel management, environmental facilities, reagents and consumables, information systems, sample management, etc. Through the 4 standards, we can strengthen the constructional standard of biobank, promote the standardization of management and operation, so as to offer samples of high quality to down-stream scientific research.

Abstract: Sarcopenia is a syndrome characterized by progressive and generalized loss of skeletal muscle mass and strength. Ageing is associated with sarcopenia, and end-stage renal disease accelerates the normal physiological muscle wasting resulting in an increasing prevalence of sarcopenia, which is named uraemic sarcopenia. There are several mechanisms that may be involved in the onset and progression of uraemic sarcopenia, such as hormones, changes in immune and muscle cells, metabolic acidosis, reducing protein intake and so on. Uraemic sarcopenia presents a high probability for morbidity and mortality, and consequently a high priority for muscle wasting prevention and treatment in these patients.

Vascular calcification is one of the most common complications and the main factor affecting prognosis of patients with chronic kidney disease. Early diagnosis, accurate evaluation and timely intervention on vascular calcification are crucial to improve prognosis of vascular calcification patients. A number of studies on serum biomarkers of vascular calcification were performed and got hopeful results. The current manuscript will review some biomarkers, such as matrix GlaProtein(MGP),osteocalcin(OC),pyrophosphate(PPi),osteoprotegerin(OPG),fibroblast growth factor23(FGF23),klotho protein, calciprotein particle(CCP),sclerostin and dickkopf1 (Dkk1), in order to provide significance for diagnosis and treatment of vascular calcification in patients with chronic kidney disease.

Sepsis is one of the most common causes of acute kidney injury (AKI) in clnical. Sepsis-associated AKI (SA-AKI) is difficult to detect in the early stage, and has a high mortality rate and poor prognosis. Its pathogenesis is complicated, with multiple factors involved,and its clinical phenotypes,disease progression, and treatment response are all potentially heterogeneous. Currently, there is no definite and effective means of intervention. This review summarized the pathophysiology of SAAKI, in order to provide a reference for further research.

Autologous arteriovenous fistula (AVF) is the lifeline for hemodialysis patients with endstage renal disease, and AVF failures are most often caused by venous stenotic lesions. Neointimal hyperplasia (NIH) is the main pathological change of venous stenotic lesions in failed AVFs, though its precise mechanism remains unclear. Vasa vasorum refers to the network of microvessels which penetrates the tunica adventitia and media of large blood vessels, supplying them with oxygen and nutrients and removing metabolic waste. This paper reviews the possible mechanisms of vasa vasorum participating in development of NIH to provide new theoretical explanations and new therapeutic targets for prevention and treatment of AVF failures.

Chronic kidney disease (CKD) has become a public health challenge worldwide and is closely associated with the risk of cardiovascular and other adverse events. How to identify the occurrence and progression of CKD early, stratify the risk of the population, and give early prevention and treatment is the focus of clinical attention. Metabolomics, a non-invasive, high-throughput assay elucidates the pathophysiological mechanisms of diseases by quantitative or semi-quantitative analysis of the abundance of metabolites and the metabolic pathways involved. Studies indicate that the metabolome of CKD patients can show significant differences with deteriorating renal function, and a variety of metabolites are closely associated with the deterioration of renal function, the risk of cardiovascular events, and even the risk of all-cause mortality in patients. Metabolomics has been successfully applied to improve the assessment of GFR and explore novel biomarkers for the risk of CKD and its complications. Furthermore, the application of metabolomics expands the understanding of the underlying pathophysiologic mechanisms of various complications during CKD and strengthens the understanding of the interactions of gut microbiome and their metabolites with CKD. This article reviews the research progression and application of metabolomics in CKD to provide novel directions for clinical diagnosis and treatment.