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.

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.

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.

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.

Tolllike Receptor 9 (TLR9) is a member of Tolllike receptor family that use pathogen associated molecule patterns (PAMPs) as ligands. It is expressed in immune cells and senses bacterial DNA ligand to induce innate immune response. Recent studies have shown that TLR9 is also expressed in several nonimmune cells，including glomerular podocyte， and uses mitochondrial DNA as ligand to activate signaling pathways that lead to cell injury. Here, we will review the roles of TLR9 in immune cells and nonimmune cells and the underlying mechanisms.

ABSTRACT A 59 year-old man suffered from diabetes for 20 years. He had hypertension and hyperuricemia, and also had complications of diabetic nephropathy which presented with proteinuria, hypoalbuminemia, and renal insufficiency. One month ago, he received xylitol with a quotidian dose of 25g for 13 days, and then acute kidney injury occurred. A renal biopsy showed glomerular nodular lesions, and interstitial fibrosis and tubular atrophy. In addition, massive depositions of double refractive crystals located in the tubules of the renal cortex in the polarized light microscopy accompanied by necrosis of the tubular epithelium. The final diagnosis was acute calcium oxalate nephropathy superimposed on diabetic nephropathy.