Objective To identify and validate the key genes of ferroptosis in phospholipase A2 receptor (PLA2R) associated membranous nephropathy through bioinformatics analysis and in vitro experiments, and to explore the potential role of ferroptosis in PLA2R associated membranous nephropathy (PMN). Methods The GSE115857 dataset obtained by retrieving the Gene Expression Omnibus (GEO) database and the ferroptosis-related genes obtained by retrieving the FerrDb database were intersected. The intersected genes were subjected to Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis. The key ferroptosis genes associated with PMN were identified by intersecting genes selected using support vector machines-recursive feature elimination and least absolute shrinkage and selection operator regression. The results were validate by real-time PCR, cell counting kit-8, Western blotting and immunofluorescence in human renal podocyte line AB 8/13 from both the control group and model group. Results A total of 25 genes related to ferroptosis of PMN were obtained, and GO and KEGG analysis showed that these genes were mainly involved in cell ferroptosis metabolism. The key ferroptosis genes of PMN obtained by machine learning method were activating transcription factor 3 (ATF3) and coiled coil domain containing 6 (CCDC6). The results of in vitro experiments showed that the human renal podocyte line AB 8/13 in the model group was significantly deformed and retracted compared with the control group. The surface area density of foot processes was significantly reduced, and the podocyte cytoskeleton was allosteric. The morphology of F-actin was disordered and the expression of synaptopodin was decreased. The cell proliferation activity was significantly decreased (P<0.05). The expression of PLA2R protein was increased (P<0.05), and the expression of GPX4 protein was decreased (P<0.01). The protein and mRNA levels of ATF3 and CCDC6 were significantly up-regulated (all P<0.05). Conclusions Ferroptosis may be one of the key mechanisms in the occurrence and development of PMN. In vitro experiments show that ATF3 and CCDC6 are the key genes in the ferroptosis of PMN podocytes, which provides new insights and ideas for the pathogenesis of PMN.

Objective To investigate the current status of vascular access team building and analysis its related factors in hemodialysis centers in China. Methods The study was a cross-sectional survey. Using a convenience sampling method, a questionnaire was designed to investigate the clinical practice of vascular access teams in 527 hemodialysis centers in China from March to April 2022. The related factors of the formation of vascular access teams and the setting up of vascular access coordinators (VAC) were analyzed by multivariate logistic regression method. Results A total of 506 valid questionnaires were recovered, with a recovery rate of 96.02%. There were 247 (48.81%) and 193 (38.14%) hemodialysis centers respectively across China that had built vascular access teams and set up VAC. Hemodialysis centers with more than 10 years of practice had higher rate of implementation than those in hemodialysis centers with practice years less or equal than 10 years in developing standardized procedures for vascular access management (χ² =8.288, P=0.004), holding continuous quality improvement meetings on vascular access (χ² =8.210, P=0.004), establishing vascular access teams (χ² =33.805, P<0.001) and setting up vascular access coordinators (χ² =16.038, P<0.001), and the difference was statistically significant. The results of multivariate logistic regression analysis showed that the number of dialysis machines (OR=2.221, 95% CI 1.118-4.415, P=0.023), the number of patients on dialysis(OR=2.946, 95% CI 1.375-6.310, P=0.005), and the establishment of VAC positions (OR=9.463, 95% CI 5.307-16.874, P<0.001), and the standardized vascular access management process (OR=3.383, 95% CI 2.012-5.687, P<0.001) were the related factors of vascular access team building. The related factors of setting up a VAC position in hemodialysis center were opening vascular access clinic (OR=2.704,95% CI 1.382-5.290, P=0.004), the formation of a vascular access team (OR=9.464, 95% CI 5.312-16.860, P<0.001), and constructing standardized procedures for vascular access management (OR=3.663, 95% CI 2.243-5.982, P<0.001). Conclusion The implementation rates of vascular access team and VAC position in hemodialysis centers were 48.81% and 38.14%, respectively. The number of dialysis machines, the number of patients on dialysis, the standardized procedures for vascular access management, the vascular access clinic, the vascular access team, and the VAC position were the relevant factors of the team building for vascular access.

Objective To explore the clinical feature and genetic variation of NPHS1 variant-associated nephropathy (NPHS1-VAN) in Chinese patients. Methods This study was a case-series analysis. Patients with NPHS1-VAN, who were treated and/or followed in the Department of Pediatrics, Nanfang Hospital, Southern Medical University between 2018 and 2023 were recruited into this study. Genotype, phenotype and their relationship were analyzed. Results Nine NPHS1-VAN patients from 8 non-consanguineous Chinese families were collected, including 5 males and 4 females. There were 7 cases with an onset age within 3 months and 2 cases with an onset age of 6 months and 13 years, respectively. Seven patients harbored compound heterozygous variants, two had homozygous variants, including 8 missense variations,3 frameshift variants, and 1 splicing site variant. Four patients in 3 families harbored missense variant c.928G>A, two of them experienced spontaneous remission of proteinuria at the age of 1 year and 2 years, respectively, another one had persistent proteinuria and entered end stage renal disease (ESRD) at 11 years old. The other one had an onset age of 6 months with no response to steroids initially. She got complete remission by tacrolimus administered, but relapse frequently and partially responded to steroids later. Two patients of this group died, one of them died of respiratory failure 3 days after birth. Excessive amniotic fluid and fetal edema were acknowledged at 28 weeks of gestational age. He harbored compound heterozygous variants of NPHS1, c.1135C>G (R379G) and c.1339G>A (E447K). His mother previously experienced fetal death at 28 weeks gestational age for her first pregnant and stillborn at 36 weeks of gestational age for her second pregnant, respectively. One patient in this study who harbored homozygous variant of c.1339G>A (E447K) presented with a mild phenotype, onset age was 13 years old and didn't progress to ESRD yet at 21 years. Thus, variant E447K was hypothesized to be weakly pathogenic, while R379G may be strongly pathogenic with a risk of death. Five novel variants were identified in this group of patients, 3 missense variants (c.1135C>G, c.1157A>T, c.3197T>A) and 2 frameshift variants (c.709_710delCT, c.3193delG). Renal biopsy was performed in 4 cases, of whom two were focal segmental glomerular sclerosis and another two were minimal change disease. Conclusions NPHS1-VAN possesses remarkable clinical and genetic heterogeneity. Five novel variants were identified. Missense variant is the most common variant type and c.928G>A is the most common one in this group of patients, in consistent with previous report in China. Children harbor c.928G>A may have a mild phenotype with possible spontaneous remission and may be response to steroids and calcineurin inhibitor. Variant c.1135C>G (R379G) may have a strong pathogenicity, and patient who harbors this variant may have a severe phenotype.

Objective To evaluate the efficacy and safety of rituximab (RTX) in children with steroid resistant nephrotic syndrome (SRNS). Methods The was a retrospective observational study. A retrospective analysis was conducted on the clinical data of 14 children with SRNS who received RTX treatment in the Department of Nephrology, Children's Hospital Affiliated to Capital Institute of Pediatrics from July 2021 to August 2023. The changes in urinary protein content, renal function, serum albumin, immunoglobulin and other indicators before and after RTX medication were compared to evaluate the clinical efficacy and safety of RTX treatment for SRNS. Results A total of 14 children with SRNS were selected for this study, with a male to female ratio of 6:8. The age of onset of kidney disease was (4.36±3.12) years, and 8 of them underwent kidney biopsy. Among them, 6 cases showed focal segmental glomerulosclerosis in renal pathology, and 2 cases showed minimal change disease. The age of 14 children who first used RTX was (8.45±3.98) years old, with a dose of 375 mg/m² and a maximum dose of 500 mg. The number of children who had used 2, 3, 4, and 5 doses of RTX was 6, 6, 1, and 1, respectively. RTX was administered orally with compound sulfamethoxazole to prevent infection. Glucocorticoids and immunosuppressants were discontinued 4.0(2.5, 6.5) months after the first dose of RTX. The median follow-up time was 10.5(6.0, 18.3) months. By the end of the 3-month, 6-month, and follow-up endpoints, the complete remission rates of kidney disease in the children were 100.0%(14/14), 85.7%(12/14), and 64.3%(9/14), respectively. Five children experienced kidney disease recurrence. Compared with before the first dose of RTX treatment, the serum albumin and height significantly increased, while body mass index significantly decreased at the end of follow-up (all P<0.05). There was no statistically significant difference in urinary protein content, renal function, and IgG (all P>0.05). During the RTX treatment, all 14 children did not experience any infusion reaction, and there were no serious infections during follow-up. One case was diagnosed with hypogammaglobulinemia. Conclusions RTX can improve the remission rate and recurrence rate of SRNS children, reduce the dosage of glucocorticoids and related drug untoward reaction, significantly improve patient height and BMI, with minimal side effects. Especially for SRNS patients who cannot be relieved by the combination of glucocorticoids and immunosuppressants, RTX may be considered.

Objective To investigate the effect of circular RNA (circRNA)_005987 on contrast-associated acute kidney injury (CA-AKI) and its mechanism, and provide new ideas for the prevention and treatment of CA-AKI. Methods CA-AKI rat models and HK-2 cell injury models were established using iopromide, and CA-AKI-related circRNA_005987 was screened based on circRNA expression chip and real-time quantitative PCR (RT-qPCR). Knockdown and overexpression of circRNA_005987 were performed in HK?2 cell model, respectively. Cell counting kit?8 (CCK-8) and Edu staining assays were used to evaluate cell proliferation. Western blotting was used to detect the protein expression of autophagy-related protein microtubule?associated protein 1 light chain 3B (LC3B), P62, beclin?1 and autophagy-related gene 14 (ATG14). Immunofluorescence staining was used to detect protein expression of LC3B. Electron microscope was used to observe the autophagosome formation. Autophagy activator rapamycin and autophagy inhibitor 3-methyladenine were used for in vitro rescue experiments to observe the changes of the above indicators. Mechanistically, bioinformatics analysis was applied to analyze the binding site among circRNA_005987, miR-129-5p and ATG14, and dual luciferase reporter assay was used to verify their interactions. CircRNA_005987 was knocked down and overexpressed in HK?2 cell model, and RT-qPCR was used to detect the expression of miR-129-5p. HK?2 cells were treated with miR-129-5p inhibitor and mimic, Western blotting was used to detect the protein expression of ATG14, and CCK8 and Edu staining assays were used to evaluate cell proliferation. Results CircRNA_005987 expression was up-regulated in vitro and vivo CA-AKI models (both P<0.05). Overexpression of circRNA_005987 inhibited cell proliferation and promoted cell autophagy, while knockdown of circRNA_005987 had opposite effects (all P<0.05). In vitro rescue experiments confirmed that circRNA_005987 inhibited cell proliferation by activating autophagy (P<0.05). The dual luciferase reporter assay suggested that there was an interaction between circRNA_005987, miR-129-5p and ATG14. Knockdown of circRNA_005987 increased miR-129-5p expression, while overexpression of circRNA_005987 inhibited miR-129-5p expression (both P<0.05). Knockdown of miR-129-5p inhibited cell proliferation, while overexpression of miR-129-5p reversed the effect (both P<0.05). Conclusion CircRNA_005987 promotes CA-AKI through activating autophagy via sponging miR-129-5p, suggesting that circRNA_005987 plays an important role in the pathological process of CA-AKI.

The study was a prospective observational study. A total of 24 patients who underwent maintenance hemodialysis (MHD) at Haidian Hospital in Beijing from May 2024 to June 2024 were included as the study subjects. The safety and efficacy of a new single-needle dialysis in MHD patients were evaluated. The reasons for using single-needle dialysis included waiting for the maturity of internal fistula(7 cases, 29.17%), autogenous arteriovenous fistula thrombosis occurred (6 cases, 25.00%), puncture difficulty occurred (7 cases, 29.17%), and pain sensitivity or elderly (4 cases, 16.67%). The results showed that the average blood flow was (155.65±5.90) ml/min, total blood volume was (35.92±2.65) L during single-needle dialysis. One patient had slight puncture leakage, and the puncture success rate was 95.83%. Relevant indicators of dialysis adequacy showed that the average urea clearance (Kt/V) was 0.90±0.42, urea reduction ratio was 58.31%±7.93%, and online real-time Kt/V monitoring average value was 0.98±0.55. The results suggest that the application of the new improved single-needle dialysis mode in MHD patients is safe and effective.

Anti-neutrophil cytoplasmic antibody-associated vasculitis (AAV) induced by anti-thyroid drugs has been reported occasionally, but methimazole-induced AAV is not as frequently reported. This case report described a 54-year-old male who developed AAV and multiple organ failure after more than 20 days of methimazole treatment. After timely discontinuation of the disease-causing drug methimazole, the patient received methylprednisolone shock, cyclophosphamide immunosuppression, renal replacement therapy, and other supportive treatments, and the disease was alleviated without recurrence.

Gaucher disease is an autosomal recessive genetic disorder, with membranoproliferative glomerulonephritis (MPGN) being a rare complication. Here we present a case of type I Gaucher disease complicated with MPGN to improve the understanding of this disease. For patients presenting with abdominal distension, hepatosplenomegaly and myelofibrosis, Gaucher disease should be considered to avoid misdiagnosis and inappropriate treatment. The detection of β-glucosidase, genetic mutation analysis and histopathological examination can play crucial roles in the diagnosis of Gaucher disease. Treatment with glucocorticoids combination with immunosuppressants can improve patient's prognosis.

Chronic kidney disease (CKD) is a significant global public health issue. In recent years, several new drugs have shown substantial efficacy in CKD treatment. Sodium-glucose cotransporter 2 inhibitors, nonsteroidal mineralocorticoid receptor antagonists, and glucagon-like peptide-1 receptor agonists improve renal outcomes in CKD patients through various mechanisms, and also demonstrate favorable effects on cardiovascular outcomes. Novel agents, including endothelin receptor antagonists, are accumulating clinical evidence for delaying kidney disease progression, with ongoing development of new therapeutic targets. This article reviewed the latest research progress of these drugs in CKD treatment, offering new perspectives and reference points for comprehensive CKD management.

Ferroptosis is a type of programmed cell death characterised by iron-dependent accumulation of lipid reactive oxygen species, which is closely related to intracellular metabolism of amino acids, lipids, and iron, and regulation of ferroptosis can intervene and treat certain diseases. Diabetic kidney disease (DKD) is a chronic microvascular complication of diabetes.Although the exact pathogenesis of DKD is not clear, the results of the existing studies have proved that ferroptosis participates in the development of diabetic kidney injury, and plays an important role in kidney tubular injury in particular, and the inhibition of ferroptosis may be one of the directions for the treatment of DKD. In recent years, researchers have conducted a lot of studies on ferroptosis through animal models of DKD, but the specific pathogenesis and therapeutic effects regarding ferroptosis have not been fully revealed. This article introduces ferroptosis and its connection with apoptosis, autophagy and other forms of cell death, as well as the main mechanisms regulating the development of ferroptosis through systematic Xc-GSH-GPX4 axis, NADPH-FSP1-CoQ10 axis, GCH1-BH4- phospholipid axis and various regulatory factors, and provides an overview of its role in kidney tubular injury of DKD. Through the review of these contents, the possibility of ferroptosis as a therapeutic target for DKD is discussed, in order to provide reference for the basic research and clinical treatment of DKD.

Piezo is a newly discovered mechanosensitive ion channel (MSC) in mammals, characterized by a unique homotrimeric three-leaf propeller-shaped structure that converts mechanical signals into biological and electrical signals, thus participating in the regulation of various physiological and pathological processes. In recent years, an increasing number of studies have demonstrated the crucial role of Piezo channel in renal physiology and pathophysiology. This article aims to provide new perspectives and targets for the prevention and treatment of renal diseases by reviewing the recent research advances in the structure, kinetics and pharmacology of Piezo channel, especially their expression and physiopathologic roles in the kidney.