To explore the potential mechanism of the rhubarb-Salvia miltiorrhiza herb pair in the intervention of diabetic kidney disease (DKD) by integrating Gene Expression Omnibus (GEO) data mining, network pharmacology, and molecular docking techniques.

Active ingredients and potential targets of rhubarb-Salvia miltiorrhiza were obtained through the Traditional Chinese Medicine Systems Pharmacology (TCMSP) database combining with the Chinese Pharmacopoeia and relevant literature. The glomerular dataset GSE30528 and the tubular dataset GSE30529 related to DKD were retrieved from the GEO database, and differential analysis was performed in the two types of tissues to screen exploratory candidate targets. Protein-protein interaction analysis was performed using the STRING database, and the target network was constructed with Cytoscape software, while GO functional annotation and KEGG pathway enrichment analysis of key targets were conducted via R language. Finally, molecular docking verification was carried out using AutoDock Vina.

From rhubarb-Salvia miltiorrhiza, a total of 90 active ingredients, 150 potential targets, and 3, 592 candidate differential targets for DKD were screened out, yielding a total of 43 intersecting targets. Topological analysis identified the core targets as EGFR, CASP3, ICAM1, KDR, and MAPK1, and the core components as emodin, aloe-emodin, danshensu, and tanshinone ⅡA. Go enrichment involved epithelial cell proliferation and apoptosis, ERK1/2 cascade reaction, and collagen-containing extracellular matrix. KEGG enrichment was mainly observed in PI3K/Akt, MAPK, integrin, and HIF-1 signaling pathway. Molecular docking showed that the binding energies of emodin and tanshinone ⅡA to the core target EGFR were -9.32 and -9.59 kcal/mol, respectively, both exhibiting favorable theoretical binding activity.

The rhubarb-Salvia miltiorrhiza herb pair may participate in the pathological processes associated with DKD through a multi-component, multi-target, and multi-pathway network. The signal networks related to emodin, tanshinone ⅡA, and EGFR can serve as candidate directions for subsequent in-vivo and in-vitro verification.

To explore the influence of dulaglutide combined with dapagliflozin on renal function and fibrosis in patients with type 2 diabetic kidney disease (T2DKD).

This study was a prospective randomized controlled trial. Consecutive patients with T2DKD admitted to our hospital from January 2024 to December 2024 were enrolled and randomly assigned to an observation group and a control group. All patients received basic routine treatment for diabetes. The control group was treated with dapagliflozin monotherapy, while the observation group received additional intervention with dulaglutide injection on the basis of dapagliflozin. Levels of renal function, renal fibrosis markers, and inflammatory factors were measured and compared between the two groups at baseline and 12-month follow-up. Adverse events during treatment were also recorded. Inter-group comparisons were performed using the t-test and Pearson χ² test.

A total of 94 patients with T2DKD were enrolled in this study, with 47 patients in the observation group and 47 in the control group. All the patients completed 12-month standardized treatment. After treatment, the estimated glomerular filtration rate (eGFR) was significantly increased in both groups compared with baseline, and post-treatment eGFR in the observation group was markedly higher than that in the control group (P<0.05). After treatment, the urine albumin-to-creatinine ratio (UACR), serum creatinine (Scr), blood urea nitrogen (BUN), renal fibrosis markers including transforming growth factor-β1 (TGF-β1), connective tissue growth factor (CTGF), kidney injury molecule-1 (KIM-1), as well as inflammatory factors including high-sensitivity C-reactive protein (hs-CRP), interleukin-1β (IL-1β), and tumor necrosis factor-α (TNF-α) were obviously decreased in both groups relative to baseline; moreover, these indicators in the observation group were significantly lower than those in the control group (P<0.05). Glycated hemoglobin (HbA1c) and fasting plasma glucose (FPG) were significantly reduced in both groups after treatment (P<0.05), whereas no statistically significant inter-group differences in HbA1c and FPG were observed after treatment. There was no significant difference in the incidence of adverse events between the two groups during the treatment period.

Dulaglutide combined with dapagliflozin can better preserve renal function, inhibit renal fibrosis, and reduce systemic inflammatory response in patients with T2DKD. Its glucose-lowering efficacy is comparable to dapagliflozin monotherapy, with favorable safety profile.

Diabetic kidney disease (DKD), as the leading cause of end-stage renal disease, involves complex pathophysiological mechanisms. In recent years, macrophage-mediated immune metabolic dysregulation has been identified as a critical driver of DKD progression, where the phenotypic switching between M1 and M2 macrophages is governed by specific metabolic reprogramming (glycolysis versus oxidative phosphorylation). Nuclear factor erythroid 2-related factor 2 (Nrf2), a core transcription factor for cellular antioxidant response, not only regulates redox homeostasis but also influences macrophage polarization, thereby exerting renoprotective effects. However, the precise molecular mechanisms by which Nrf2 modulates macrophage metabolic reprogramming to affect polarization within the DKD microenvironment remain elusive. This review aims to systematically elucidate the molecular mechanisms of Nrf2 in regulating metabolic reprogramming and polarization of macrophage in DKD, providing new insights and potential therapeutic targets for the precision treatment of DKD.

Volume status assessment plays a central role in the clinical management of hemodialysis patients, and its accuracy directly affects patients′ prognosis and survival rate. In recent years, relevant research on artificial intelligence models in this field has demonstrated application potential. Precise assessment of volume status can be achieved by analyzing multi-dimensional clinical data, providing a basis for personalized treatment. This paper reviews the application of artificial intelligence and its combination with traditional volume assessment methods in volume evaluation for hemodialysis patients, and discusses their advantages, limitations, and development directions.

Patients on maintenance hemodialysis are in a state of persistent low-grade microinflammation. The accumulation of pro-inflammatory cytokines and middle-large molecular uremic toxins is closely associated with cardiovascular events, protein-energy wasting, and deteriorated quality of life. Conventional hemodialysis has limited capacity to remove middle-large molecular inflammatory mediators, and may even aggravate inflammatory responses due to bioincompatibility. Based on adsorption mechanism, hemoperfusion combined with conventional dialysis can eliminate uremic toxins such as β-microglobulin and inflammatory mediators including interleukin-6 and tumor necrosis factor-α, and to some extent regulate immune cell activation and ameliorate the imbalance of immune cell subsets. This article reviews the pathological basis of microinflammation in maintenance hemodialysis patients, as well as the mechanism, combined modalities, and clinical research progress of hemoperfusion, so as to provide references for the optimization of blood purification strategies.

Chronic kidney disease-associated pruritus (CKD-aP) is a common yet long-overlooked complication among patients with end-stage renal disease. CKD-aP can significantly affect patients′ quality of life, sleep, and mood, reduce dialysis adherence, and is closely associated with an increased risk of mortality. In recent years, with deeper understanding of its pathogenesis and advances in the research and development of therapeutic drugs, CKD-aP has been redefined from a conventional accompanying "symptom" to an independent clinical disorder requiring active identification and systematic intervention. This article systematically reviewed CKD-aP from the perspectives of epidemiology, pathogenesis, diagnostic procedures, assessment scales, stratified management strategies, and advances in pharmaceutical research. It focuses on introducing the characteristics and clinical application value of various pruritus assessment tools as well as their applications in the research and development of κ-opioid receptor agonists, and discusses stratified management regimens based on pruritus severity. The aim is to improve clinicians′ ability to identify and standardly manage CKD-aP and improve patients′ prognosis.

Chronic hyperglycemia serves as the core initiating trigger of diabetic kidney disease (DKD). Through the interactive regulation and cascade amplification of multiple pathways including disordered glucose and lipid metabolism, abnormal renal hemodynamics, oxidative stress, chronic low-grade inflammation, and excessive activation of the lectin pathway in the complement system, it continuously damages the structure and function of podocytes, subsequently induces glomerulosclerosis and renal tubulointerstitial fibrosis, and mediates the onset and progressive deterioration of DKD. As one of the three major activation pathways of the complement system, the lectin pathway was discovered most recently, and research interest in it has been rising year by year. Characterized by its ability to initiate activation without antibodies, this pathway acts as a critical mediator linking innate immune defense and inflammatory responses, and plays a central role in the pathophysiological processes of DKD. This paper reviews the mechanisms and research progress of the core components of the lectin pathway of the complement system in DKD, discussing their feasibility as therapeutic targets for providing new insights for basic research, clinical prevention and treatment of DKD.

The gut-kidney axis is a core pathway mediating signal communication between the gut and the kidney, and the gut microbiota acts as a key regulatory node of the gut-kidney axis by regulating bile acid metabolism. Bile acid metabolism not only participates in various pathophysiological processes such as glucose and lipid metabolism, intestinal microecological balance, and inflammatory immune regulation, but also affects renal function through gut-kidney axis-mediated signaling pathways, and is involved in the progression of dyslipidemia, atherosclerosis, chronic kidney disease (CKD), etc. CKD can induce gut-kidney axis imbalance, resulting in intestinal microbiota disturbance and abnormal bile acid profiles. The disrupted bile acid profiles can promote CKD progression through mechanisms such as accelerating renal fibrosis, interfering with lipid metabolism, and triggering micro-inflammation. At present, relevant evidence is mostly derived from animal experiments and clinical observational association studies, and the causal regulatory relationship between bile acid metabolism and CKD remains to be further verified.

The closed-loop BOPPPS teaching model consists of six links: bridge-in, objective, pre-assessment, participatory learning, post-assessment, and summary. It features clear teaching hierarchy and prominent interactivity, meets the developmental demands of medical specialty teaching reform, and has demonstrated application advantages in medical education practice. Nephrotic syndrome represents a key and difficult content in clinical teaching for nephrology postgraduates. Traditional teaching modes still predominate at present, and systematic practical summaries regarding standardized BOPPPS teaching for nephrotic syndrome are scarce. This paper systematically combed the theoretical framework, implementation strategies and application effects of the BOPPPS teaching model in nephrotic syndrome clinical teaching for nephrology postgraduates. Questionnaire analysis of 16 postgraduates indicated that this model can effectively improve the quality of clinical teaching.