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 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.

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.

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.

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.

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.

Lactic acidosis results from the accumulation of lactate and protons in the body fluids, and is often associated with poor clinical outcomes. Mortality is increased by a factor of nearly three times when lactic acidosis accompanies lowflow states or sepsis, and the higher the lactate level, the worse the outcome. Although hyperlactatemia is often attributed to tissue hypoxia, it can result from other mechanisms. Control of the triggering conditions is the only effective means of treatment. However, advances in understanding its pathogenesis could lead to new therapies. This paper overview the pathogenesis of lactic acidosis, as well as the diagnosis and management.

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.

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.

ＴRenal fibrosis is the main pathological change of chronic kidney disease with various causes. It has been found that histone acetyltransferases (HATs) mediated epigenetic modification was tightly associated with the occurrence and development of renal fibrosis. The p300／CBP family consisting of the highly homologous adenovirus E1Aassociated 300 kDa protein (p300) and cAMP responsive element binding protein (CREB) binding protein (CBP) is one of the major members of the HATs families. This paper reviewed the structure, function, and the role of p300／CBP in renal fibrosis, attempting to provide new targets and ideas for the prevention and treatment of renal fibrosis.

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.

Focal segmental glomerulosclerosis (FSGS) is a common glomerular disease leading to end stage renal disease, and podocyte injury is the main cause of it.The pathogenesis of podocyte injury in idiopathic FSGS is still unknown. Idiopathic FSGS is easy to relapse and the overall prognosis is poor，except for glucocorticoids and calcinurin inhibitors, there are still lack of effective treatments.Several literatures have reported that rituximab (RTX) can obtain beneficial effects in idiopathic FSGS. As a B cell depletion agent, how RTX plays a role in treatment of idiopathic FSGS, its immunological efficacy and cytoprotective mechanism are still being study. Therefore, based on the drug characteristics of RTX, this paper reviews the main clinical studies and related researches in the field of podocyte injury in recent years ,presenting the immunological mechanism and podocyte protective mechanism of RTX in the treatment of idiopathic FSGS.

Podocytes are terminally differentiated cells that reside on the outer surface of the glomerular basement membrane and play a key role in maintaining the structure and function of the glomerular filtration barrier.Podocyte dysfunction,injury or loss is a common and decisive cause of various glomerular diseases.Minimal change disease (MCD) and focal segmental glomerulosclerosis (FSGS) are the major podocytopathies.This review is focus on recent studies on the mRNA prole of podocyte and genetic mutations on structural and functional molecules in podocyte.We will highlight advances in the understanding of novel molecular mechanisms of podocyte damage.