Background. Traditional Chinese medicine (TCM) has long been used to treat chronic kidney disease (CKD) in Asia. Its effectiveness and safety for CKD treatment have been confirmed in documented studies. However, the prescription rule of formulae for Chinese medicinal herbs is complicated and remains uncharacterized. Thus, we used data mining technology to evaluate the treatment principle and coprescription pattern of these formulae in CKD TCM treatment. Methods. Data on patients with CKD were obtained from the outpatient system of a TCM hospital. We established a Chinese herb knowledge base based on the Chinese Pharmacopoeia and the Chinese Materia Medica. Then, following extraction of prescription information, we deweighted and standardized each prescribed herb according to the knowledge base to establish a database of CKD treatment formulae. We analyzed the frequency with which individual herbs were prescribed, as well as their properties, tastes, meridian tropisms, and categories. Then, we evaluated coprescription patterns and assessed medication rules by performing association rule learning, cluster analysis, and complex network analysis. Results. We retrospectively analyzed 299 prescriptions of 166 patients with CKD receiving TCM treatment. The most frequently prescribed core herbs for CKD treatment were Rhizoma Dioscoreae (Shanyao), Spreading Hedyotis Herb (Baihuasheshecao), Root of Snow of June (Baimagu), Radix Astragali (Huangqi), Poria (Fulin), Rhizoma Atractylodis Macrocephalae (Baizhu), Radix Pseudostellariae (Taizishen), and Fructus Corni (Shanzhuyu). The TCM properties of the herbs were mainly being warm, mild, and cold. The tastes of the herbs were mainly sweet, followed by bitter. The main meridian tropisms were Spleen Meridian of Foot‐Taiyin, Liver Meridian of Foot‐Jueyi, Lung Meridian of Hand‐Taiyin, Stomach Meridian of Foot‐Yangming, and Kidney Meridian of Foot‐Shaoyin. The top three categories were deficiency‐tonifying, heat‐clearing, and dampness‐draining diuretic. Conclusion. Using an integrated analysis method, we confirmed that the primary TCM pathogeneses of kidney disease were deficiency and dampness‐heat. The primary treatment principles were tonifying deficiency and eliminating dampness‐heat.

Background: In chronic kidney disease (CKD), there is evidence of loss of function and fibrosis in the progression of tubular epithelial cells; however, the cellular heterogeneity and underlying molecular mechanisms are not well defined. Knowledge of the diversity among tubular cells is essential for precision medicine therapy. Methods: We subjected renal cells from CKD patients to single‐cell RNA sequencing with a focus on tubular epithelial populations. Through unsupervised clustering, a computational pipeline that includes metabolic pathway scoring and pseudotemporal trajectory inference combined with machine learning classification, our analysis enabled the characterization of intratumoral cellular diversity and metabolic states coupled to differentiation trajectories. We analyzed segment‐specific markers (SLC34A1, SLC5A2, LRP2, CUBN, ALDOB, and GATM) and metabolic enzymes (glycolysis and TCA cycle enzymes) in cell subsets. Results: Tubular cells showed marked heterogeneity and metabolic reprogramming from oxidative phosphorylation to glycolysis, clustering as OXPHOS‐high, glycolytic, dormant, and intermediate cell states. The expression of segment‐specific markers was differentially retained and lost, reflecting maintenance of fate as well as dedifferentiation. Pseudotemporal analysis demonstrated progressive cellular transitions driven by the expression of critical genes such as MALAT1 and ANXA1. Proximal tubule cells constituted ∼70% of the profiled cells with different transcriptomic signatures. Moderate classification results were obtained using a machine learning approach (ROC AUC = 0.673). Conclusions: This work furnishes a molecular atlas of tubular epithelial cell heterogeneity in CKD, highlighting metabolic reprogramming and transdifferentiation as key processes driving tubular dysfunction and fibrosis. These results also revealed potential therapeutic targets to retain tubular function and ameliorate the progression of CKD.

Plant‐derived polyphenols possess broad anti‐inflammatory activities and may benefit chronic inflammatory diseases. XuanBi is a traditional Chinese medicine formula containing orally absorbable polyphenolic constituents and is used to treat rheumatoid arthritis (RA). This study investigated its absorbable components and potential mechanisms associated with synovial inflammatory hyperplasia. XuanBi was evaluated in collagen‐induced arthritis (CIA) rats and rheumatoid arthritis synovial fibroblasts (RASFs). Constituents in the decoction and rat serum were characterized by high‐performance liquid chromatography coupled with quadrupole‐Orbitrap mass spectrometry (HPLC‐Q‐Orbitrap‐MS). Predicted targets were intersected with synovial differentially expressed proteins (DEPs), followed by network pharmacology, Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses, and experimental validation. Twenty‐six absorbable constituents were identified, including catechin, quercetin, baicalein, and wogonin, together with 14 candidate proteins associated with RA synovial pathology. Enrichment analysis implicated extracellular matrix (ECM)–receptor interaction, focal adhesion, and interleukin‐17 (IL‐17) signaling. Medium‐ and high‐dose XuanBi reduced joint swelling, synovial hyperplasia, and inflammatory infiltration in CIA rats. In RASFs, XuanBi inhibited proliferation, migration, and invasion. It also downregulated fibronectin 1 (FN1) and caveolin 1 (CAV1), reduced phosphorylation of SRC, focal adhesion kinase (FAK), and FYN, decreased integrin alpha 2b (ITGA2B) ⁺ /integrin beta 1 (ITGB1) ⁺ cells, and reduced interleukin‐1 beta (IL‐1β), interleukin‐6 (IL‐6), tumor necrosis factor alpha (TNF‐α), matrix metallopeptidase 3 (MMP3), and matrix metallopeptidase 9 (MMP9). Overall, XuanBi exerted anti‐inflammatory and anti‐synovial‐hyperplasia effects in experimental RA, accompanied by changes in proteins associated with these pathways, supporting the potential involvement of these pathways and warranting further mechanistic and clinical investigation.