AimTo explore the symptom distress and quality of life status of patients with Chronic Kidney Disease (CKD) Stage 5 undergoing hemodialysis in China, and their correlation.MethodsThe Dialysis Symptom Index (DSI) and the Kidney Disease Quality of Life Short Form (KDQOL-SF™ 1.3), two widely used assessment tools for hemodialysis patients, were used for evaluation.ResultsThe patients reported an average of 13 symptoms. The most common symptoms were worrying (99.7%), sexual dysfunction (>90%), and trouble falling asleep (90.8%). The KDQOL-SF™ 1.3 showed that patients had lower scores in dimensions such as “Burden of Kidney Disease” and “Work Status,” while they had higher scores in the “Dialysis Staff Encouragement” and “Role Limitations - Emotional” dimensions. Univariate analysis revealed that age, education level, employment status, dialysis frequency, dialysis modality, primary disease, multiple comorbidities, complications (renal anemia), and polypharmacy were significantly associated with the total DSI score. Spearman’s rank correlation analysis showed a negative correlation between the total DSI score and each dimension of KDQOL-SF™ 1.3, with the strongest correlation found with the “Symptom/Problem List” dimension. Multivariate linear regression analysis indicated that age, education level, dialysis duration, dialysis modality, and primary disease (diabetic nephropathy) were independent influencing factors for the total DSI score. After controlling for confounding factors, the total DSI score remained independently negatively correlated with multiple dimensions of KDQOL-SF™ 1.3.ConclusionsSymptom distress is negatively correlated with quality of life in Chinese CKD Stage 5 hemodialysis patients. Clinical attention should be given to symptom screening and management.

BACKGROUND Diabetic kidney disease (DKD) is a leading cause of end-stage renal disease. Integrative approaches combining traditional Chinese medicine and Western pharmacotherapy have shown potential benefits. AIM To evaluate the efficacy and safety of Bailing capsules (BCs) combined with SGLT2is in DKD treatment. METHODS Randomized controlled trials (RCTs) were retrieved from China National Knowledge Infrastructure, Wanfang, VIP, PubMed, Web of Science, EMBASE, and Cochrane Library up to September 14, 2025. Data extraction and quality assessment were performed independently by two reviewers using the Cochrane risk of bias tool. Meta-analysis was conducted with Stata 18.0, and trial sequential analysis (TSA) was applied to assess the robustness of evidence. RESULTS Fourteen RCTs involving 1919 patients were included. Compared with SGLT2is alone, BC plus SGLT2is significantly improved clinical efficacy [relative risk (RR) = 1.157, 95%CI: 1.102-1.216]; reduced fasting blood glucose [weighted mean difference (WMD) = -0.729, 95%CI: -0.976 to -0.482] and glycated hemoglobin (WMD = -0.680, 95%CI: -0.768 to -0.592) levels; altered renal function markers, including serum creatinine [SCr; standardized mean difference (SMD) = -1.033, 95%CI: -1.258 to -0.808], blood urea nitrogen (WMD = -1.158, 95%CI: -1.537 to -0.779), and beta 2-microglobulin (WMD = -1.237, 95%CI: -1.471 to -1.002) levels; and reduced 24-hour urinary protein levels (SMD = -1.329, 95%CI: -1.801 to -0.857). No significant increase in the incidence of adverse events was observed (RR = 0.939, P = 0.767). Subgroup analysis suggested that the optimal BC dosage was 1.0-3.0 g three times daily. TSA confirmed the reliability of the evidence for a reduction in SCr. CONCLUSION BC combined with SGLT2is appears to be effective and safe for improving glycemic control and renal function in DKD patients. Further high-quality, multicenter RCTs are warranted to validate these findings.

ObjectiveTo compare cardiovascular and renal benefits and safety of GLP-1RAs, SGLT2is, and nsMRAs in T2D-CKD using network meta-analysis.MethodsRCTs published through 7 August 2026 were systematically identified. A frequentist random-effects network meta-analysis was performed. Evidence certainty was assessed with CINeMA.ResultsA total of 21 RCTs involving 51,899 patients were included. Compared with placebo, nsMRAs were associated with lower risks of the major kidney composite outcome and hospitalization for heart failure (HHF), whereas SGLT2is were associated with lower risks of major adverse cardiovascular events (MACE), the major kidney composite outcome, and HHF. GLP-1RAs were associated with lower risks of MACE, the major kidney composite outcome, HHF, all-cause mortality, and cardiovascular death. Between-class indirect comparisons suggested a lower estimated risk of the major kidney composite outcome with SGLT2is than with GLP-1RAs (RR 0.77, 95% CI 0.64–0.91) or nsMRAs (nsMRAs versus SGLT2is: RR 1.28, 95% CI 1.10–1.50). The estimated risk of HHF was also lower with SGLT2is than with nsMRAs (nsMRAs versus SGLT2is: RR 1.28, 95% CI 1.01–1.63). For cardiovascular death, the indirect estimate suggested a lower risk with GLP-1RAs than with SGLT2is (SGLT2is versus GLP-1RAs: RR 1.28, 95% CI 1.03–1.58), whereas the comparison between nsMRAs and GLP-1RAs did not reach statistical significance (RR 1.24, 95% CI 0.99–1.56). No statistically significant between-class differences were identified for MACE or all-cause mortality. All between-class comparisons were based exclusively on indirect evidence. Safety analyses showed higher risks of hyperkalemia with nsMRAs and genital infections with SGLT2is than with placebo. Sensitivity analyses broadly supported the main findings. Confidence in the evidence was mostly low to moderate, primarily because of indirectness.ConclusionIn patients with T2D-CKD, all three drug classes reduced several cardiorenal outcomes versus placebo. Between-class indirect comparisons suggested more favorable relative-effect estimates for SGLT2is on major kidney outcomes and HHF in selected comparisons, and for GLP-1RAs on cardiovascular death. No clear between-class difference was observed for MACE. Because the network lacked head-to-head comparisons between active drug classes, these findings and treatment rankings should be interpreted cautiously. Direct comparative and combination-therapy trials are needed to guide individualized treatment selection.Systematic Review Registrationhttps://www.crd.york.ac.uk/PROSPERO/view/CRD420251150683, identifier CRD420251150683.

Diabetic nephropathy (DN) is a leading cause of chronic kidney disease. Salvianolic acid A (SAA) has shown promising therapeutic potential against DN, yet its underlying mechanisms and precise molecular targets remain incompletely elucidated. Potential targets of SAA were predicted using SwissTargetPrediction and SuperPred, with its drug-like properties evaluated by ADMET analysis. Diabetic nephropathy (DN)-related targets were collected from GEO, CTD, and GeneCards databases. Shared targets underwent GO and KEGG enrichment analyses. Core targets were identified through topological analysis in Cytoscape, machine learning, and Mendelian randomization validation. Molecular docking and dynamics simulations assessed the binding affinity and stability between SAA and core targets. Single-cell RNA sequencing data revealed their cell type-specific expression in kidney tissues. Experimental validation was performed using an in vitro high glucose-induced podocyte injury model analyzed by RT-qPCR. The intersection of 212 drug targets with 5,097 disease targets yielded 134 potential therapeutic targets for salvianolic acid A in DN. Machine learning and Mendelian randomization further identified eight targets with causal relationships to DN. Molecular docking demonstrated strong binding affinities of salvianolic acid A to the domains of FYN, AKR1B1, TNF, GALK1, HMGCR, MAP2K2, SCN4A, and ITGA5. Single-cell analysis revealed distinct expression patterns across different renal cell types. In vitro experiments demonstrated that SAA effectively protected podocytes from HG-induced injury. SAA alleviates diabetic nephropathy through multi-target mechanisms, influencing key genes involved in disease progression. This study provides a systematic elucidation of the therapeutic basis for SAA and supports its further clinical development.

Fine particulate matter (PM2.5) is an established environmental risk factor for chronic kidney disease, yet the molecular pathways linking PM2.5 exposure to diabetic nephropathy (DN) progression remain to be elucidated. This study employs a multi-omics causal inference framework to identify and characterize candidate genetic and epigenetic mediators that may underlie this association. Utilizing a curated set of PM2.5-annotated genes, we performed summary-data-based Mendelian randomization (SMR) analyses, integrating expression, protein, and methylation quantitative trait loci (eQTLs, pQTLs, mQTLs) with DN genome-wide association study (GWAS) summary statistics. Bayesian colocalization was used to distinguish shared from distinct causal variants. The expression of prioritized genes was validated in an independent DN transcriptomic dataset (GSE96804) and through in vitro PM2.5 exposure experiments. A predictive nomogram for DN risk was subsequently developed and evaluated. Transcript-level SMR identified ten PM2.5-associated genes (e.g., TNF, NOS2, DUSP1) with genetically predicted causal effects on DN susceptibility. Bayesian colocalization revealed strong evidence for a shared causal variant only at EIF2AK3 (PP.H4 = 0.90). Methylation analysis revealed 48 CpG sites significantly associated with DN risk, mapping to 28 genes, with TNF methylation showing the strongest effect. Multi-omics integration and protein–protein interaction analysis highlighted TNF as a central hub within an enriched inflammatory network. Furthermore, mQTL-eQTL SMR showed that hypermethylation at cg11484872 suppressed TNF, whereas methylation at cg14968860 and cg18091275 upregulated DUSP1 and NOS2, respectively, establishing bidirectional epigenetic regulation of these genes. In DN kidney tissue, TNF and NOS2 were upregulated while DUSP1 was downregulated, and these changes were recapitulated in cellular models following PM2.5 exposure. A nomogram based on NOS2 and TNF yielded an AUC of 0.766 in the training set and 0.726 in an independent external cohort (GSE142153). Our integrative analysis identifies a PM2.5-responsive epigenetic-gene regulatory network involving TNF, NOS2, and DUSP1 that may represent candidate mediators of PM2.5-related DN progression. These findings nominate molecular candidates for environmental kidney injury and highlight potential biomarkers for risk stratification.

The global incidence and prevalence of kidney diseases continue to rise, posing a serious public health challenge. SIRT6 is an NAD⁺-dependent histone deacetylase with broad essential regulatory roles across various pathophysiological processes, including DNA repair, chromatin accessibility, telomere stability, and glycolipid metabolism. As an epigenetic regulator specifically expressed in kidney tissues, SIRT6 serves as a central mediator of kidney homeostasis. Notably, accumulating evidence has implicated aberrant SIRT6 expression in the onset and development of various kidney diseases, such as acute kidney injury, diabetic kidney disease, hypertensive nephropathy, renal fibrosis, and renal cell carcinoma. In the present review, we provide an overview of the sirtuin family, systematically characterize the enzymatic activities and critical biological functions of SIRT6, and discuss its molecular mechanisms across various kidney diseases, focusing on its cell type-specific functions. We further summarize the latest research advances in SIRT6-targeted modulators for improving kidney diseases and analyze the challenges associated with their clinical application. Overall, we highlight SIRT6 as a highly promising novel target in the treatment and prevention of kidney diseases, with strong potential for clinical translation.

Introduction Progressive tubulointerstitial injury plays a critical role in the progression of diabetic kidney disease (DKD), but the epigenetic mechanisms driving this process remain largely unclear. Objectives This study aimed to investigate the role of the histone deacetylase SIRT6 in renal tubular epithelial cells (TECs) during DKD progression and to explore its potential as a therapeutic target. Methods We employed digital spatial profiling (DSP) to perform spatially resolved mRNA quantification in proximal renal tubular tissue from DKD patients. Additionally, we used genetic and pharmacological approaches in DKD mouse models to assess the effects of SIRT6 deficiency or overexpression on renal injury. Mechanistic studies included RNA-sequencing (RNA-seq) and Cleavage Under Targets and Tagmentation (CUT&Tag) sequencing, which to identify SIRT6-regulated genes and epigenetic modifications. Results Our findings revealed a significant reduction of SIRT6 in TECs from DKD patients, with its expression inversely correlating with disease severity. TEC-specific SIRT6 deficiency worsened renal injury and proteinuria in DKD mice, whereas SIRT6 overexpression or pharmacological activation provided renoprotection. Mechanistically, SIRT6 directly repressed Nlrp3 transcription by deacetylating histone 3 lysine 9 (H3K9), thereby inhibiting NLRP3 inflammasome activation and subsequent TEC injury. Conclusion These findings highlight SIRT6 as a protective epigenetic factor in DKD and suggest its potential utility for disease stratification, early therapeutic intervention, and precision medicine.

Introduction: Renal fibrosis is an endpoint event of various progressive chronic kidney diseases (CKD), but there are no effective antifibrotic treatments. Yiqi Qingre Gao (YQQRG) has shown potential in alleviating CKD, although its exact mechanism of action remains uncertain. This study aims to evaluate the impact of YQQRG on renal fibrosis and to explore the molecular pathways involved.Methods: The study employed a unilateral ureteral obstruction (UUO) mouse model, followed by a 2-week course of YQQRG treatment. Renal function was assessed through measurements of serum creatinine (SCr) and blood urea nitrogen (BUN). Kidneys were collected for histological and molecular biology analysis. To identify the detailed mechanisms, network pharmacology, RNA sequencing (RNA-Seq), transforming growth factor-beta1 (TGF-β1)-stimulated human renal proximal tubular epithelial (HK-2) cells, and molecular docking were used.Results: YQQRG treatment significantly improved renal function, pathological damage, and renal fibrosis in UUO mice. Ten blood-entering components and 403 potential targets of YQQRG were identified by liquid chromatography-mass spectrometry (LC-MS) and network pharmacology. 20,107 targets of renal fibrosis were revealed by RNA-Seq of kidneys from the control and UUO groups. The results of the KEGG pathway enrichment analysis of YQQRG and renal fibrosis were combined, which showed that YQQRG’s renoprotective effects were strongly associated with the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) signaling pathway. Experimental validation further confirmed that YQQRG suppressed the PI3K/AKT pathway in the renal tissues of UUO mice; the addition of the PI3K/AKT agonist reversed the antifibrotic effects of YQQRG in TGF-β1-stimulated HK-2 cells. Furthermore, molecular docking indicated that YQQRG’s primary active components exhibited a strong binding affinity to critical targets.Discussion: This study initially demonstrated that YQQRG improved renal function and kidney injury in UUO mice by revealing its antifibrotic mechanism, and it operates through the inhibition of the PI3K/AKT pathway, which highlights YQQRG as a potential therapeutic option for treating CKD.

Diabetic vascular complications include diabetic macroangiopathy and diabetic microangiopathy. Diabetic microangiopathy is characterised by impaired microvascular endothelial function, basement membrane thickening, and microthrombosis, which may promote renal, ocular, cardiac, and peripheral system damage in diabetic patients. Therefore, new preventive and therapeutic strategies are urgently required. Sirt1, a member of the nicotinamide adenine dinucleotide-dependent histone deacetylase class III family, regulates different organ growth and development, oxidative stress, mitochondrial function, metabolism, inflammation, and aging. Sirt1 is downregulated in vascular injury and microangiopathy. Moreover, its expression and distribution in different organs correlate with age and play critical regulatory roles in oxidative stress and inflammation. This review introduces the background of diabetic microangiopathy and the main functions of Sirt1. Then, the relationship between Sirt1 and different diabetic microangiopathies and the regulatory roles mediated by different cells are described. Finally, we summarize the modulators that target Sirt1 to ameliorate diabetic microangiopathy as an essential preventive and therapeutic measure for diabetic microangiopathy. In conclusion, targeting Sirt1 may be a new therapeutic strategy for diabetic microangiopathy.

Ethnopharmacological relevance: Diabetic nephropathy (DN) is the leading cause of end-stage kidney disease and currently there are no specific and effective drugs for its treatment. Podocyte injury is a detrimental feature and the major cause of albuminuria in DN. We previously reported Tangshen Formula (TSF), a Chinese herbal medicine, has shown therapeutic effects on DN. However, the underlying mechanisms remain obscure. Aim of the study: This study aimed to explore the protective effect of TSF on podocyte apoptosis in DN and elucidate the potential mechanism. Materials and methods: The effects of TSF were assessed in a murine model using male KKAy diabetic mice, as well as in advanced glycation end products-stimulated primary mice podocytes. Transcription factor EB (TFEB) knockdown primary podocytes were employed for mechanistic studies. In vivo and in vitro studies were performed and results assessed using transmission electron microscopy, immunofluorescence staining, and western blotting. Results: TSF treatment alleviated podocyte apoptosis and structural impairment, decreased albuminuria, and mitigated renal dysfunction in KKAy mice. Notably, TSF extracted twice showed a more significant reduction in proteinuria than TSF extracted three times. Accumulation of autophagic biomarkers p62 and LC3, and aberrant autophagic flux in podocytes of DN mice were significantly altered by TSF therapy. Consistent with the in vivo results, TSF prevented the apoptosis of primary podocytes exposed to AGEs and activated autophagy. However, the anti-apoptosis capacity of TSF was countered by the autophagy-lysosome inhibitor chloroquine. We found that TSF increased the nuclear translocation of TFEB in diabetic podocytes, and thus upregulated transcription of its several autophagic target genes. Pharmacological activation of TFEB by TSF accelerated the conversion of autophagosome to autolysosome and lysosomal biogenesis, further augmented autophagic flux. Conversely, TFEB knockdown negated the favorable effects of TSF on autophagy in AGEs-stimulated primary podocytes. Conclusions: These findings indicate TSF appears to attenuate podocyte apoptosis and promote autophagy in DN via the TFEB-mediated autophagy-lysosome system. Thus, TSF may be a therapeutic candidate for DN.

BackgroundAs a damage-associated molecular pattern protein, high mobility group box 1 (HMGB1) is associated with kidney and systemic inflammation. The predictive and therapeutic value of HMGB1 as a biomarker has been confirmed in various diseases. However, its value in diabetic kidney disease (DKD) remains unclear. Therefore, this study aimed to investigate the correlation between serum and urine HMGB1 levels and DKD progression.MethodsWe recruited 196 patients with type 2 diabetes mellitus (T2DM), including 109 with DKD and 87 T2DM patients without DKD. Additionally, 60 healthy participants without T2DM were also recruited as controls. Serum and urine samples were collected for HMGB1 analysis. Simultaneously, tumor necrosis factor receptor superfamily member 1A (TNFR-1) in serum and kidney injury molecule (KIM-1) in urine samples were evaluated for comparison.ResultsSerum and urine HMGB1 levels were significantly higher in patients with DKD than in patients with T2DM and healthy controls. Additionally, serum HMGB1 levels significantly and positively correlated with serum TNFR-1 (R2 = 0.567, p<0.001) and urine KIM-1 levels (R2 = 0.440, p<0.001), and urine HMGB1 has a similar correlation. In the population with T2DM, the risk of DKD progression increased with an increase in serum HMGB1 levels. Multivariate logistic regression analysis showed that elevated serum HMGB1 level was an independent risk factor for renal function progression in patients with DKD, and regression analysis did not change in the model corrected for multiple variables. The restricted cubic spline depicted a nonlinear relationship between serum HMGB1 and renal function progression in patients with DKD (p-nonlinear=0.007, p<0.001), and this positive effect remained consistent across subgroups.ConclusionSerum HMGB1 was significantly correlated with DKD and disease severity. When the HMGB1 level was ≥27 ng/ml, the risk of renal progression increased sharply, indicating that serum HMGB1 can be used as a potential biomarker for the diagnosis of DKD progression.

PURPOSE:To evaluate the key topics and emerging trends in the field of cardiorenal syndrome type 4 (CRS-4) by bibliometrics and visual analysis.METHODS:Citespace, VOSviewer, and Bibliometrix package were used to analyze the collected data from the Web of Science Core Collection, including publication trends, leading countries, active authors and institutions, co-cited references, journals, and keyword analysis.RESULTS:Finally, 2267 articles were obtained. From 2004 to 2022, the number of publications was increasing year by year. A total of 735 authors from 543 institutions in 94 countries/regions participated in the publication of CRS-4 field, which were mostly from North America and Europe. Most of the co-cited references were reviews or guidelines from kidney/heart specialist journals or top journals. The journals concerning nephrology had a higher academic influence in this field. Oxidative stress and inflammation remained hot topics in CRS-4 research, as well as uremic toxins. Fibroblast growth factor 23 and klotho were emerging trends in recent years. Sodium glucose cotransporter 2 (SGLT2) inhibitors were the latest frontier hot spots. Future research advances may pay more attention to the prevention and prognosis assessment of CRS-4.CONCLUSION:Our study provides some key information for scholars to determine the direction of future research.

Sirtuins, which are NAD+-dependent class III histone deacetylases, are involved in various biological processes, including DNA damage repair, immune inflammation, oxidative stress, mitochondrial homeostasis, autophagy, and apoptosis. Sirtuins are essential regulators of cellular function and organismal health. Increasing evidence suggests that the development of age-related diseases, including kidney diseases, is associated with aberrant expression of sirtuins, and that regulation of sirtuins expression and activity can effectively improve kidney function and delay the progression of kidney disease. In this review, we summarise current studies highlighting the role of sirtuins in renal diseases. First, we discuss sirtuin family members and their main mechanisms of action. We then outline the possible roles of sirtuins in various cell types in kidney diseases. Finally, we summarise the compounds that activate or inhibit sirtuin activity and that consequently ameliorate renal diseases. In conclusion, targeted modulation of sirtuins is a potential therapeutic strategy for kidney diseases.

Clear cell renal cell carcinoma (ccRCC) characterised by its diversity and a tendency to defy standard therapeutic approaches. Amidst the advent of immunotherapy, it has become imperative to pinpoint prognostic indicators of the tumour microenvironment (TME) influence the efficacy of treatments. Employing single-cell RNA sequencing (scRNA-seq), this research delved into the diverse landscape of ccRCC, uncovering its complex underpinnings and pinpointing molecular avenues for therapeutic intervention. We constructed a prognostic model using 101 machine learning algorithms and integrated data from multiple cohorts, including TCGA, ICGC, and microarray datasets. The model's efficacy was assessed using the Concordance Index (C-index), and further analyses included pseudotime analysis of tumour cells, mutation analysis and correlation analysis between the prognostic model and tumour immunity. The prognostic model, combining Lasso regression and survival Support Vector Machine (SVM), demonstrated robust discrimination with a C-index of 0.650. Investigation into the TME uncovered pronounced associations between the presence of immune cell infiltrates and patient outcomes, with a notable emphasis on the impact of CCL2-expressing neoplastic cells. The GO Biological Processes (GOBP) encompass the regulation of endothelial cell maturation, the formation of endothelial layers, the enhancement of gene expression controlled by Notch receptors, and the development of endothelial barriers. The research effectively pinpointed critical prognostic markers and crafted a forecasting model that achieved a C-index of 0.650, highlighting the significant impact of immune cell infiltration, especially CCL2+ neoplastic cells, on ccRCC patient prognosis.

BACKGROUND:The treatment of clear-cell renal cell carcinoma (ccRCC) remains challenge. Chemokines laid impact on the proliferation and metastasis of cancer cells. The objective was to identify the chemokine-related genes and construct a prognostic model for ccRCC. METHODS:Bulk transcriptomic data (n = 531), single-cell RNA sequencing (scRNA-seq) dataset GSE159115, and other validation cohorts were acquired from the Cancer Genome Atlas Program (TCGA) and GEO databases. All clustering analysis was conducted by Seurat R package. Gene set enrichment analysis (GSEA), immune infiltration analysis, single nucleotide variations (SNV) analysis, and predictive response analysis of immunotherapy/chemotherapy were conducted. 786-O and A498 cell lines were cultured and applied into CCK-8, Western blot, and RT-qPCR kits. RESULTS:Univariate Cox analysis was used to screen out chemokine-related genes related to survival. ZIC2, SMIM24, COL7A1, IGF2BP3, ITPKA, ADAMTS14, CYP3A7, and AURKB were identified and applied for the construction of the prognostic model. High-risk group had a poorer prognosis than the low-risk group in each dataset. Memory CD8+ T cells, macrophages, and memory B cells were higher in the high-risk group, while the content of basophils was higher in the low-risk group. Bortezomib_1191, Dactinomycin_1911, Docetaxel_1007, and Daporinad_1248 were more sensitive to high-risk groups than low-risk groups. Moreover, we found that IGF2BP3 significantly elevated in both 786-O and A498 cell lines resistance to sunitinib. Knockdown of IGF2BP3 markedly reduced ccRCC cell migration and viability. CONCLUSION:Our study has yielded a novel prognostic model of chemokine-related genes based on comprehensive transcriptional atlas of ccRCC patients, shedding light on the significant impact of the tumor microenvironment on biology and immunotherapy response of ccRCC. We identified IGF2BP3 as a pivotal regulator in regulating ccRCC resistance to sunitinib.

Artemisinin, an antimalarial traditional Chinese herb, is isolated from Artemisia annua. L, and has shown fewer side effects. Several pieces of evidence have demonstrated that artemisinin and its derivatives exhibited therapeutic effects on diseases like malaria, cancer, immune disorders, and inflammatory diseases. Additionally, the antimalarial drugs demonstrated antioxidant and anti-inflammatory activities, regulating the immune system and autophagy and modulating glycolipid metabolism properties, suggesting an alternative for managing kidney disease. This review assessed the pharmacological activities of artemisinin. It summarized the critical outcomes and probable mechanism of artemisinins in treating kidney diseases, including inflammatory, oxidative stress, autophagy, mitochondrial homeostasis, endoplasmic reticulum stress, glycolipid metabolism, insulin resistance, diabetic nephropathy, lupus nephritis, membranous nephropathy, IgA nephropathy, and acute kidney injury, suggesting the therapeutic potential of artemisinin and its derivatives in managing kidney diseases, especially the podocyte-associated kidney diseases.

病例 赵某某,女,38 岁,主因"间断双下肢水肿11 年余,加重1周"入院.患者11年前无明显诱因出现双下肢水肿,某医院查尿常规:PRO( + + +)、ERY( + +),24 h尿蛋白5. 37 g,Scr 48 μmol/L、Alb 33 g/L.临床诊断:慢性肾小球肾炎,肾病综合症.肾脏病理诊断:膜增生性肾小球肾炎.