Renal replacement therapy (RRT) is widely used in the intensive care unit (ICU), but its application in patients with acute kidney injury (AKI) still lacks unified standards. In November 2024, the French Society of Intensive Care Medicine, in collaboration with the French Pediatric Critical Care and Emergency Group, published an evidence-based guideline for both adult and pediatric patients with AKI. This guideline systematically updates the management strategies for RRT in the ICU. It emphasizes the deferral of RRT initiation in the absence of emergent indications, the equivalence of outcomes across different RRT modalities, and the feasibility of peritoneal dialysis under resource constraints, while specifying the initiation indications for pediatric patients with hyperammonemia. At the implementation level, it proposes a conservative dosing regimen for adults and an individualized approach for pediatric patients. Furthermore, it does not recommend heparin locking for patients at high risk of bleeding, highlighting the importance of blood volume management and daily weaning assessments. This article reviews and interprets the main recommendations of the guideline, and discusses their implications for the standardized management of RRT in China.

Over the past two decades, the widespread application of genetic testing technologies, particularly the clinical implementation of next-generation sequencing, has profoundly reshaped the understanding of genetic kidney diseases in children. This technological advancement has significantly improved the diagnostic yield for genetic kidney diseases in both adults and children, accelerating the discovery and identification of pathogenic genes, while continuously expanding and refining the genotype-phenotype correlations of classical renal disorders. These advances have driven the updating and reclassification of genetic kidney diseases, shifting the clinical management paradigm from a traditional phenotype-oriented approach to a precision medicine model centered on genetic variants, pathophysiological mechanisms, and molecular etiologies. Based on the renewed understanding of the pathogenesis and clinical heterogeneity of genetic kidney diseases, this article systematically reviews and analyzes the evolving genotype-phenotype spectra of several typical pediatric genetic kidney diseases. Furthermore, it proposes recommendations regarding the indications for genetic testing in clinical practice of pediatric nephrology, aiming to provide a reference for the precise diagnosis and treatment of these disorders.

To investigate the role of nuclear factor-E2-related factor 2 (Nrf2) in high glucose-induced epithelial-mesenchymal transition (EMT) in human renal tubular epithelial cells (human kidney-2, HK-2).

Cultured HK-2 cells were divided into: normal glucose group (NG group, 5.5 mmol/L glucose), high glucose group (HG group, 30 mmol/L glucose), high glucose plus Nrf2 siRNA transfection group (HG+ siNrf2 group), high glucose plus negative control siRNA transfection group (HG+ NC group), high glucose plus N-acetylcysteine group (HG+ NAC group), and high glucose plus tert-butylhydroquinone group (HG+ TBHQ group). The expression levels of α-smooth muscle actin and fibronectin were examined using Western blotting, quantitative real-time PCR, and immunofluorescence. Intracellular and mitochondrial reactive oxygen species (ROS) levels were measured with specific assay kits.

Compared with the NG group, α-smooth muscle actin expression was significantly upregulated in the HG group. In contrast, the protein and mRNA expression levels of α-smooth muscle actin and fibronectin were markedly downregulated in the HG+ TBHQ and HG+ NAC groups compared to the HG group (all P<0.05). Furthermore, both the protein and mRNA expression levels of α-smooth muscle actin and fibronectin were significantly higher in the HG+ siNrf2 group than in the HG+ NC group (all P<0.05). Compared with the NG group, both intracellular and mitochondrial ROS levels were significantly higher in the HG group (all P<0.05). In contrast, the levels of intracellular and mitochondrial ROS were markedly lower in the HG+ TBHQ and HG+ NAC groups compared to the HG group (all P<0.05).

Activation of the Nrf2 signaling pathway inhibited high glucose-induced ROS production and EMT in human renal tubular epithelial cells.

To systematically investigate the mechanism of Jisheng Shenqi Pills (JSP) in treating chronic renal failure (CRF) with network pharmacology and molecular docking methods.

Step 1, Component and target screening: The active ingredients and their corresponding targets of JSP were screened using the Traditional Chinese Medicine Systems Pharmacology (TCMSP) database and the High-throughput Experiment and Referenced Bioinformatics (HERB) database. Disease-related targets for CRF were retrieved from the Gene Cards (GeneCards), Online Mendelian Inheritance in Man (OMIM), and Disease Gene Network (DisGeNET) databases. And the intersecting targets between the drugs and the disease were identified. Step 2, Network construction and enrichment analysis: The protein-protein interaction (PPI) network was constructed using the Search Tool for Retrieval of Interacting Genes/Proteins (STRING) database to identify core target genes. And the "herb-component-target-disease" network was visualized using the Cytoscape software. Functional enrichment analysis was then performed with the Gene Ontology (GO) database, and pathway enrichment with the Kyoto Encyclopedia of Genes and Genomes (KEGG) database. Step 3, Validation by molecular docking: The molecular docking validation between the key active ingredients and core targets was performed using the AutoDock Vina software.

A total of 102 active ingredients of JSP were identified, corresponding to 232 potential targets. A total of 2, 153 targets were associated with CRF, resulting in 138 overlapping targets between the drug and the disease. Network analysis revealed that quercetin, kaempferol, wogonin, baicalein, and oleic acid were the key active ingredients. The core targets primarily included AKT1, TNF, IL6, MAPK1, TP53, CASP3, and BCL2. GO analysis suggested that the targets were mainly involved in inflammation, oxidative stress, apoptosis, and immune regulation. KEGG analysis showed enrichment in pathways related to AGE-RAGE, TNF, IL-17, PI3K-Akt, and lipids-atherosclerosis. Molecular docking confirmed the strong binding affinity between key components and core targets.

JSP may delay CRF progression by regulating key targets (AKT, MAPK, TNF) and signaling pathways (AGE-RAGE, PI3K-Akt) via flavonoid ingredients (quercetin, kaempferol), thereby exerting anti-inflammatory, antioxidant, inhibiting-apoptosis, and immunomodulatory effects. This illustrates the multi-component, multi-target, and multi-pathway advantages of traditional Chinese medicine (TCM) formulas, providing a theoretical basis for further mechanistic studies.

Spliced X-box-binding protein 1 (XBP1s), a core transcription factor in the endoplasmic reticulum stress signaling pathway, regulates protein folding and degradation, influences the functions of immune cells such as B cells, T cells, and dendritic cells, and plays a key role in inflammatory responses and immune-mediated diseases. As such, it has emerged as a potential therapeutic target for autoimmune disorders. Targeted therapeutic strategies against XBP1s, including small-molecule drugs and RNA interference technologies, are currently under development. Targeted therapeutic strategies against XBP1s, including small-molecule drugs and RNA interference technologies, are currently under development. This review summarized the pivotal roles and molecular mechanisms of XBP1s in autoimmune diseases and discussed the application prospect of targeted intervention of XBP1s in the precision therapy of autoimmune diseases.

Apolipoprotein L1-associated kidney disease is a renal disorder mediated by risk variants in the apolipoprotein L1 (APOL1) gene, predominantly manifesting as focal segmental glomerulosclerosis (FSGS). Currently, there is no specific therapy, and the efficacy of existing non-specific treatment regimens remains suboptimal. With the deepening understanding of the pathogenic mechanisms underlying APOL1 G1/G2 risk variants and the recently reported p. T272I variant, targeted therapeutic agents, such as small-molecule inhibitors, antisense oligonucleotides, and Janus kinase inhibitors, have successively entered clinical investigation. This article reviews the latest advances in APOL1-associated kidney disease, spanning from genetic mechanisms to targeted therapeutics.

Membranous nephropathy (MN) is a glomerular disease characterized by diffuse thickening of the glomerular basement membrane and subepithelial immune complex deposition. Traditionally MN is diagnosed via renal biopsy pathology. In recent years, the discovery of some target antigens has revolutionized the diagnosis and treatment of MN. Precise typing based on antigen classification has significantly improved diagnostic specificity and prognostic assessment capabilities. Research has confirmed that clinical heterogeneity of different antigens is significant: M-type phospholipase A2 receptor (PLA2R) and thrombospondin type-1 domain-containing 7A (THSD7A) may be associated with the risk of malignancy; neural epidermal growth factor-like 1 (NELL1) is associated with multifactorial pathogenic characteristics; exostosin glycosyltransferase 1/2 (EXT1/2) indicates subtypes of lupus nephritis; while semaphorin 3B (SEMA3B) and neuron-derived neurotrophic factor (NDNF) point to childhood MN and syphilis-related MN, respectively. In terms of treatment, traditional immunosuppressive regimens (such as rituximab) remain the core therapy, but novel targeted therapies (including antibody clearance technology, chimeric antigen receptor T-cell therapy, and immunoadsorption) have shown potential by precisely eliminating pathogenic antibodies or B cells, although their efficacy and safety still require long-term verification. This article systematically reviewed the clinical significance of the antigens spectrum and therapeutic advancements of MN, providing a reference for individualized diagnosis and treatment.

Lupus nephritis (LN) is one of the most common and severe complications of systemic lupus erythematosus (SLE). It is a major contributor to both morbidity and mortality among SLE patients, and can progress to end-stage renal disease, thereby significantly impairing prognosis. In recent years, with the deepening understanding of the pathogenesis of LN, novel therapeutic agents and strategies have emerged rapidly, making personalized and precision medicine a research hotspot. This review summarized the latest advances in the treatment of LN, aiming to provide a robust reference for optimizing clinical practice and guiding future research directions.