High glucose induces podocyte ferroptosis through BAP1/SLC7A11 pathway.

Background: Ferroptosis plays an important role in the development of diabetic nephropathy (DN). However, its specific regulatory mechanisms remain unclear.

Methods: MPC5 cells were cultured in high glucose (HG) medium to stimulate the HG environment in vitro.

Plasma thrombin-activatable fibrinolysis inhibitor and the 1040C/T polymorphism are risk factors for diabetic kidney disease in Chinese patients with type 2 diabetes.

Background: Inflammatory and hemostatic disorders in diabetic microangiopathy (DMA) can be linked to thrombin-activatable fibrinolysis inhibitor (TAFI) and its own gene polymorphisms. Thus, the study aimed to investigate the associations of plasma TAFI and gene polymorphisms with DMA in Chinese patients with type 2 diabetes (T2D).

Methods: Plasma TAFI of 223 patients with T2D was measured, and the genotypes and alleles of the 1040C/T, 438G/A, and 505G/A polymorphisms of the gene were analyzed.

Plasma D-dimer levels are associated with disease progression in diabetic nephropathy: a two-center cohort study.

Background: This study aimed to investigate the relationship between plasma D-dimer levels, clinicopathological features, and clinical outcomes in patients with biopsy-proven diabetic nephropathy (DN).

Methods: A total of 137 patients with biopsy-proven DN were enrolled in this two-center cohort study. Patients were stratified into tertiles based on plasma D-dimer levels.

Excess selenium intake is associated with microalbuminuria in female but not in male among adults with obesity: Results from NHANES 2009-2018.

Introduction: Selenium is a critical trace element with antioxidant activities that has been related to the preservation of kidney function. Few studies, however, have looked at the effects of excess selenium on kidneys. The purpose of the present study was performed to investigate the relationship between dietary selenium intake and the prevalence of microalbuminuria in American adults with obesity.

Urinary N-acetyl-β-d-glucosaminidase-creatine ratio is a valuable predictor for advanced diabetic kidney disease.

Background: Many biomarkers show high diagnostic values for diabetic kidney disease (DKD), but fewer studies focus on the predictive assessment of DKD progression by blood and urinary biomarkers.

Aim: This study aims to find powerful risk predictors and identifying biomarkers in blood and urine for DKD progression.

Methods: A total of 117 patients with type 2 DKD including early and advanced stages and their laboratory parameters were statistically assessed.

Stratification of diabetic kidney diseases data-independent acquisition proteomics-based analysis of human kidney tissue specimens.

Aim: The aims of this study were to analyze the proteomic differences in renal tissues from patients with diabetes mellitus (DM) and diabetic kidney disease (DKD) and to select sensitive biomarkers for early identification of DKD progression.

Methods: Pressure cycling technology-pulse data-independent acquisition mass spectrometry was employed to investigate protein alterations in 36 formalin-fixed paraffin-embedded specimens. Then, bioinformatics analysis was performed to identify important signaling pathways and key molecules.

LncRNA Hoxb3os protects podocytes from high glucose-induced cell injury through autophagy dependent on the Akt-mTOR signaling pathway.

Background: Diabetic nephropathy (DN) is in the first place of the causes that lead to end-stage renal disease in the world. Thus, it is urgent to develop a novel diagnostic or therapeutic strategy that could stop the progression of diabetic nephropathy.

Methods: RNA-sequencing was conducted in high glucose (HG)-treated MPC5 cells (podocytes).

Role of Th22 Cells in Human Viral Diseases.

Naive CD4 T cells can differentiate into different cell subsets after receiving antigen stimulation, which secrete corresponding characteristic cytokines and thereby exert biological effects in various diseases. Th22 cells, a novel subset of CD4 T cells, are different from Th1, Th2, Th17, and Treg cell subsets, which have been discovered in recent years. They can express CCR4, CCR6, and CCR10 molecules and secrete IL-22, IL-13, and TNF-α.

Mesenchymal Stem Cells Attenuate Renal Fibrosis via Exosomes-Mediated Delivery of microRNA Let-7i-5p Antagomir.

Background: Renal fibrosis is a chronic and progressive process affecting kidneys in chronic kidney disease (CKD). Mesenchymal stem cells-derived exosomes (MSCs-Exo) have been shown to alleviate renal fibrosis and injury, but the mechanism of MSCs-Exo-induced renal protection remains unknown.

Methods: In this study, MSCs were transfected with let-7i-5p antagomir (anti-let-7i-5p), and then exosomes were isolated from the transfected MSCs to deliver anti-let-7i-5p oligonucleotides to inhibit the level of let-7i-5p in kidney tubular epithelial cells (NRK-52E).

iTRAQ-based comparative proteomics analysis reveals specific urinary biomarkers for various kidney diseases.

Proteome studies for multiple renal diseases is bare. Using isobaric tags for relative and absolute quantitation labeling, many differentially expressed proteins (DEPs) were identified in acute kidney injury (AKI), AKI + chronic kidney disease (CKD), diabetic CKD and nondiabetic CKD with or without IgA nephropathy (IgAN). Comparative analysis indicated that 34, 35, 17, 91 and 14 unique DEPs were found in AKI, AKI + CKD, CKD, diabetic CKD and nondiabetic CKD.

Upregulation of miRNA-1228-3p alleviates TGF-β-induced fibrosis in renal tubular epithelial cells.

Background: Chronic kidney disease (CKD) has become a major public health issue, which can lead to renal fibrosis regardless of the initial injury. It has been previously reported that miRNA-1228-3p was correlate with the progression of kidney fibrosis. However, the mechanism by which miRNA-1228-3p regulates renal fibrosis remains unclear.

New-Onset Diabetes Mellitus in Patients with Idiopathic Membranous Nephropathy Undergoing Tacrolimus and Low-Dose Corticosteroid Therapy.

Background: Idiopathic membranous nephropathy (IMN) is the most common cause of nephrotic syndrome in adults. Although various studies have demonstrated the efficacy of tacrolimus combined with corticosteroids for treating IMN, both tacrolimus and corticosteroids have been shown to be diabetogenic, particularly following organ transplantation. Furthermore, the frequency and risk factors for new-onset diabetes mellitus (NODM) in IMN patients treated with tacrolimus plus low-dose corticosteroids remain unclear.

Coexistence of Fabry disease with IgM nephropathy: A case report.

Rationale: Coexistence of Fabry disease and IgM nephropathy is rare. The varying severity and unapparent clinical manifestation of Fabry disease makes it difficult to recognize when coexisting with another more prevalent cause of nephropathy requiring electron microscopy and genetic testing to confirm their coexistence.

Patient Concerns: A 54-year-old female presented with proteinuria without any clinical signs or family history of Fabry disease.

Krüppel‑like factor 4 ameliorates diabetic kidney disease by activating autophagy via the mTOR pathway.

Diabetic kidney disease (DKD) is diagnosed increasingly frequently and represents a serious threat to human health. Krüppel‑like factor 4 (KLF4) has aroused attention due to its potential effect on podocytes and in ameliorating proteinuria associated with glomerulopathy. The purpose of the present study was to investigate the potential role of KLF4 in DKD.

Comparison of the Effects of Indobufen and Warfarin in a Rat Model of Adenine-Induced Chronic Kidney Disease.

BACKGROUND Worldwide, the treatment of patients with chronic kidney disease (CKD) remains a challenge as warfarin treatment can be associated with severe adverse events related to bleeding. Alternative anticoagulants that can be used in CKD remain to be identified. This study aimed to compare the effects of indobufen, a new antiplatelet agent, with warfarin in a rat model of adenine-induced CKD.

Autophagy activity and expression pattern of autophagy-related markers in the podocytes of patients with lupus nephritis: association with pathological classification.

Objective: To identify the significance of autophagy in lupus nephritis (LN).

Methods: The number of autophagosomes in podocytes was counted and the expression of multiple molecular markers associated with autophagy was evaluated in LN specimens: in renal biopsy specimens from 90 patients with LN and 15 healthy controls, autophagosomes in podocytes were counted using transmission electron microscopy and the expression levels of four autophage related proteins including Beclin-1, microtubule-associated protein light chain 3 (LC3), autophagy-related gene 7 (Atg7), and UNC-51-like kinase 1 (ULK1) were measured using immunohistochemistry.

Results: The number of autophagosomes in patients with LN types III, IV, and combined V-IV type were significantly higher than in controls (p < 0.

Exosome secreted from adipose-derived stem cells attenuates diabetic nephropathy by promoting autophagy flux and inhibiting apoptosis in podocyte.

Background: It is confirmed that adipose-derived stem cells (ADSCs) transplantation effectively relieves kidney fibrosis and type 2 diabetes disease in mice. Currently, exosome from urine-derived stem cells (USCs) can protect type 1 diabetes-mediated kidney injury and attenuate podocyte damage in diabetic nephropathy (DN). Exosome derived from USCs has evolved into the strategy for DN treatment, but the role of ADSCs-derived exosome (ADSCs-Exo) in DN remains unclear.

Inhibition of high mobility group box 1 (HMGB1) attenuates podocyte apoptosis and epithelial-mesenchymal transition by regulating autophagy flux.

Background: Podocyte injury, characterized by podocyte hypertrophy, apoptosis, and epithelial-mesenchymal transition (EMT), is the major causative factor of diabetic nephropathy (DN). Autophagy dysfunction is regarded as the major risk factor for podocyte injury including EMT and apoptosis. High mobility group box 1 (HMGB1) is involved in the progression of DN through the induction of autophagy.

Tripterygium glycoside protects diabetic kidney disease mouse serum-induced podocyte injury by upregulating autophagy and downregulating β-arrestin-1.

Background: Diabetic kidney disease (DKD), one of the most common causes of end-stage renal disease(ESRD), remains prevalent in many populations. Podocyte loss and apoptosis play a crucial role in the progression of DKD. Tripterygium glycoside (TG), a widely used Chinese herb, exerted comprehensive protective effects on preventing DKD progression.

Acute kidney injury in cancer patients: A nationwide survey in China.

Cancer patients have a high risk for acute kidney injury (AKI); however, the incidence, severity, and risk factors of malignancy-related AKI (MR-AKI) are unclear. This study aimed to assess MR-AKI risk factors and provide reliable data for AKI prevention, diagnosis, and management in China. This cross-sectional study analysed data from 44 academic and local hospitals in China.

STIM promotes the epithelial-mesenchymal transition of podocytes through regulation of FcγRII activity in diabetic nephropathy.

Background: Diabetic nephropathy (DN) is a serious complication in diabetic patients and has been considered as the main cause of end-stage renal disease. However, there are no studies on the role of stromal interaction molecule (STIM) and its two subtypes, STIM1 and STIM2, in the epithelial-to-mesenchymal transition (EMT) of podocytes induced by diabetic kidney disease (DKD). The present study suggests for the first time that STIM inhibition decreases DKD-induced EMT.

Tripterygium glycoside protects against puromycin amino nucleoside‑induced podocyte injury by upregulating autophagy.

Tripterygium glycoside (TG), an active ingredient of the widely used Chinese herb Tripterygium wilfordii Hook F, has immunosuppressive and anti‑inflammatory effects. Previous studies have indicated that TG is a potentially effective therapeutic option to treat nephrotic syndrome. The mechanism underlying the therapeutic effect of TG, including its effect on autophagy and apoptosis in podocyte injury, remains to be fully elucidated.

The novel involvement of podocyte autophagic activity in the pathogenesis of lupus nephritis.

Background: Lupus nephritis (LN) is one of the most common and severe complications in Systemic lupus erythematosus patients, and the mechanism underlining the pathogenesis of LN is still unknown. Autophagy plays vital roles in maintaining cell homeostasis and is involved in the pathogenesis of many diseases. In this study, we investigated the role of autophagy in the progression of LN.