Diabetic kidney disease (DKD) is a major cause of end-stage renal disease worldwide. Its pathogenesis is highly complex and involves dysfunction across multiple renal cell types and metabolic pathways, thereby underscoring the urgent need for novel therapeutic strategies. In recent years, renal metabolic reprogramming has been increasingly recognized as a central driver of DKD progression. This review systematically examines the mechanisms of metabolic reprogramming in different renal cell types and highlights their contribution to renal injury. Particular emphasis is placed on the ability of natural products (including glycosides, terpenoids, flavonoids, alkaloids, and polysaccharides) to confer renal protection by modulating key regulatory nodes of metabolic reprogramming. Through these mechanisms, natural products enhance mitochondrial function, suppress aberrant glycolysis, and improve hypoxia-related responses. Collectively, these findings not only underscore the therapeutic potential of natural products in targeting renal metabolic reprogramming but also provide a theoretical foundation and potential molecular targets for the development of novel DKD treatment strategies.

BackgroundDiabetic kidney disease (DKD) is characterized by sustained tubular inflammation. Tetrandrine (Tet), a major bioactive alkaloid of Stephania tetrandra S. Moore, has shown renoprotective potential, but its upstream inflammatory target remains unclear.MethodsMale KK-Ay mice received Tet (10, 20, or 40 mg/kg/day) for 12 weeks. Biochemical indices, renal histopathology, single-nucleus RNA sequencing, immunohistochemistry, immunofluorescence, and western blotting were assessed. Mechanistic validation in palmitic acid (PA)-stimulated HK-2 cells included immunofluorescence, western blotting, molecular docking, 100-ns molecular dynamics simulation, cellular thermal shift assay (CETSA), and co-immunoprecipitation.ResultsTet improved metabolic and renal injury indices, alleviated renal histopathological damage, and reduced inflammatory responses in KK-Ay mice. Single-nucleus RNA sequencing revealed bidirectional transcriptional remodeling in proximal tubular cells, including downregulation of a subset of inflammation- and tubular injury-associated genes. Molecular docking predicted plausible binding poses of Tet with TLR4, NF-κB RelA, and NLRP3, and the Tet–TLR4 complex remained stable during simulation. CETSA indicated increased TLR4 thermal stability, while co-immunoprecipitation suggested reduced TLR4–MyD88 association. In kidney tissue and PA-stimulated HK-2 cells, Tet reduced TLR4 expression, nuclear phosphorylated p65 accumulation, NLRP3-associated signaling, and inflammatory protein expression.ConclusionTet attenuates DKD and is associated with TLR4 engagement, reduced TLR4–MyD88 coupling, and suppression of NF-κB/NLRP3-associated inflammatory signaling in proximal tubular cells.

Membranous nephropathy (MN) is a common pathologic subtype of nephrotic syndrome in adults. Current clinical treatment strategies for MN are limited and are associated with high incidence rates of adverse reactions and risk of recurrence. Consequently, Traditional Chinese Medicine (TCM) has gradually emerged as an alternative option for patients. In recent years, TCM has accumulated substantial clinical experience in the management of MN. This review summarizes the latest research progress on TCM interventions in MN, aiming to provide additional evidence-based medical support for its clinical treatment. The proposed mechanisms of TCM in MN primarily involve immune regulation, anti-inflammation, podocyte protection, and anti-fibrosis, as well as modulation of lipid metabolism and the renal-intestinal microecosystem.

Autoimmune diseases (ADs) are a group of conditions characterized by an overactive immune response that damages one or more organs or tissues of the body. Emerging evidence highlights a critical association between reduced abundance of beneficial Clostridium and the pathogenesis of ADs. Studies show that certain Clostridium, such as Clostridium butyricum (CB) and Faecalibacterium prausnitzii (FP), are almost depleted in multiple ADs. This depletion is associated with impaired immune homeostasis, disrupted intestinal barrier integrity, and heightened inflammation. In diseases such as inflammatory bowel disease (IBD), rheumatoid arthritis (RA), and type 1 diabetes (T1D), restoration of Clostridium species or their metabolites may alleviate disease severity. Mechanistically, Clostridium probiotics may modulate ADs via multiple therapeutic mechanisms, including regulating gut microbiota composition, replenishing beneficial metabolites to restore intestinal barrier integrity, correcting dysregulated immune cell differentiation and homeostasis, and balancing pro- and anti-inflammatory cytokine levels. Our review synthesizes current evidence to delineate the immunomodulatory mechanisms by which Clostridium and its metabolites influence ADs. These findings underscore the therapeutic potential of Clostridium-based interventions in reestablishing immune-metabolic equilibrium in ADs.

Chronic kidney disease (CKD) is a significant global public health issue. However, the burden of CKD by etiology and trends over time remains inadequately studied. Data from the Global Burden of Disease Study 2021 (GBD 2021) were analyzed, including cases by region, etiology, age, and sex. Metrics included age-standardized incidence rate (ASIR), age-standardized mortality rate (ASMR), age-standardized prevalence rate (ASPR), disability-adjusted life years (DALYs), and age-standardized DALYs rate (ASDR) between 1990 and 2021. The Joinpoint regression analysis was used to calculate the average annual percentage change (AAPC), and age-period-cohort (APC) analysis was performed to assess trends. In 2021, CKD posed a substantial global burden, with 673,722,703 cases and 19,935,038 new cases. The incidence rate was 233.6 with an AAPC of 0.634. CKD caused 1,527,639 deaths, corresponding to a mortality rate of 18.5 and an AAPC of 0.745. DALYs associated with CKD totaled 44,453,684, with an AAPC of 0.322. CKD burden was primarily attributed to diabetes mellitus type 2 (DMT2), hypertension, and unspecified causes, affecting individuals aged 50 years and older. ASIR and ASPR were higher among females, while males had higher ASMR and ASDR. At regional and national levels, the incidence of CKD was positively correlated with the socio-demographic index (SDI), while mortality, DALYs, and prevalence negatively correlated with SDI. APC analysis revealed an elevated mortality risk (Net Drift = 0.3), increasing with age and over successive periods. Birth cohort analysis indicated higher mortality risks among individuals born after 1992. The global burden of CKD continued to rise due to aging populations, increasing risk factors, and improved detection. While some regions showed success in reducing CKD mortality, widening disparities demanded urgent attention. Early-stage disease and modifiable risks offered prevention opportunities, but realizing this required sustained healthcare investment, especially in resource-limited settings. Therefore, coordinated efforts addressing both risk factors and disease management would be essential to reduce its growing burden.

Renal fibrosis represents the final common pathological pathway of nearly all chronic kidney disease (CKD), yet effective therapeutic options remain profoundly limited. Rehmanniae Radix, a botanical drug in Traditional Chinese Medicine (TCM), has a long history of use for its nephroprotective properties. However, a systematic, mechanism-based understanding of how its natural products combat renal fibrosis is conspicuously absent. Herein, we present a comprehensive review to dissect the multi-component, multi-target, and multi-pathway mechanisms through which the major active ingredients of Rehmanniae Radix ameliorate renal fibrosis. Our analysis reveals that these natural products, including Acteoside (also known as Verbascoside), Catalpol, and Rehmannioside A, converge upon the inhibition of the canonical TGF-β1/Smad signaling pathway—a master regulator of fibrosis. This analysis focuses primarily on evidence from preclinical (in vivo and in vitro) models, as rigorous clinical data on the efficacy of these specific constituents remain limited. Furthermore, they exert potent anti-inflammatory and antioxidant effects via the modulation of pivotal signaling nodes such as NF-κB, Nrf2, and TLR4. Critically, this review illuminates unique and novel mechanisms, including the enhancement of autophagy by Acteoside and the targeted inhibition of the AT1R/MAPK14/IL-17 axis by Rehmannioside A in hypertensive nephropathy. By elucidating this intricate pharmacological network, this review not only decodes the scientific basis for the nephroprotective effects of Rehmanniae Radix but also provides a theoretical foundation for the development of novel anti-fibrotic therapies and identifies promising molecular targets for future investigation.

Objectives:Global diabetes rates are rising sharply, driving a parallel increase in diabetic kidney disease (DKD) - a key diabetic complication. This trend poses mounting public health and economic burdens worldwide. Current therapies remain inadequate, making DKD progression a pressing unmet need. This review aims to assess the efficacy and molecular mechanisms of food-medicine homologous herbs for DKD treatment. Methods:A comprehensive literature search was conducted across multiple databases (PubMed, Web of Science, Cochrane Library, and Embase) from inception to March 2025, using keywords including "diabetic kidney disease", and "traditional Chinese medicine". The search was meticulously designed to cover relevant research extensively. Data extraction focused on herb names, bioactive compounds, experimental models, therapeutic effects, and molecular targets. Findings:This review highlights 29 food-medicine homologous herbs with proven safety and efficacy in DKD. These herbs alleviate immune-inflammatory responses by modulating NF-κB, interleukins, TNF-α, chemokines, and adhesion molecules. They also reduce mitochondrial and non-mitochondrial ROS production, improving oxidative stress via Keap1/Nrf2/ARE, AMPK/SIRT, and NF-κB pathways. Renal fibrosis is suppressed through targeting fibrosis markers and regulating TGF-β/Smad and Notch signaling. Additionally, these herbs inhibit the AGEs/RAGE axis, correct gut dysbiosis, reduce apoptosis, activate autophagy, inhibit ferroptosis, and modulate microRNAs, collectively exerting renoprotective effects in DKD. Conclusions:Food-medicine homologous herbs demonstrate properties that align well with medical nutrition therapy principles, offering novel adjunctive therapeutic options for DKD.

Diabetic kidney disease (DKD) is a common microvascular complication of diabetes. With the continuous rise in the prevalence of diabetes, it has become the primary cause of end-stage renal disease. Currently, there are no effective clinical treatments available to reverse the progression of DKD. Stephania tetrandra S. Moore, a traditional Chinese medicine, has demonstrated significant value in the prevention and treatment of DKD due to its active components. This study focuses on exploring the molecular mechanisms through which the primary active components of S. tetrandra, tetrandrine/sinomenine and fangchinoline, exert renal protective effects via multiple pathways, including regulating inflammatory responses, antagonizing oxidative stress, improving glomerular endothelial function, modulating podocyte damage, and intervening in lipid metabolism disorders. These findings provide a theoretical basis for the development of novel therapeutic agents for DKD.

Diabetic kidney disease (DKD), a grave microvascular complication of diabetes, is the primary cause of end-stage renal disease. Despite advances in conventional therapies, their limited efficacy underscores the urgent need for novel, multi-target intervention strategies. Macrophage infiltration and the subsequent chronic microinflammation are central to the pathogenesis of renal injury in DKD. A diverse array of natural bioactive compounds are emerging as promising therapeutic agents, capable of modulating these inflammatory pathways. This review investigates the mechanisms underlying the attenuation of DKD progression by six major classes of natural compounds, such as glycosides, diterpenoids, and alkaloids, among others, through the targeting of macrophage infiltration. Collectively, this synthesis offers a compelling case for developing natural product-based, multiple-target strategies to combat DKD. Collectively, this synthesis builds a compelling case for developing multi-target therapeutic strategies derived from natural products to combat DKD.

ETHNOPHARMACOLOGICAL RELEVANCE:Jianpi Qushi Heluo formula (JQHF) is an evidence-based herbal formula based on "Fangji Huangqi Decoction" in the classic of traditional Chinese medicine (TCM) synopsis of the Golden Chamber. Its effectiveness in reducing idiopathic membranous nephropathy (IMN) proteinuria, edema and other clinical symptoms and improving kidney injury has been confirmed by clinical trials and animal experiments. These results demonstrate the critical significance of reducing podocyte injury by regulating mitophagy through integrating ethnopharmacology. AIM OF THE STUDY:This study aimed to explore the protective effects of JQHF on podocyte injury in IMN, focusing on its role in promoting PINK1-dependent mitophagy to inhibit reactive oxygen species (ROS) mediated activation of the NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome. MATERIALS AND METHODS:The main components of JQHF were identified by ultra-performance liquid chromatography combined with quadrupole time-of-flight mass spectrometry (UPLC-Q-TOF/MSE). Passive Heymann nephritis (PHN) was induced in rats using anti-Fx1A antiserum, while podocyte injury in vitro was stimulated with sublytic complement C5b-9 (sC5b-9). The PHN rats were treated with JQHF, and autophagy inhibitor 3-methyladenine (3-MA) combined with JQHF was used for pathway verification, and Benazepril served as a positive control. In vitro, podocytes were exposed to palmitic acid (PA, a ROS inducer) and N-acetylcysteine (NAC, a ROS scavenger). Further, we silenced the expression of PINK1 in podocytes model and intervened with JQHF-containing serum. Renal function was assessed through biochemical analyses and histopathology. Mitochondrial function was measured by detecting mitochondrial membrane potential (MMP), ROS levels as well as mitochondrial ultrastructure. The expression of podocyte structural proteins (desmin, nephrin, podocin) and inflammasome-related markers (NLRP3, caspase-1, IL-1β, IL-6) was analyzed to assess podocyte injury and inflammasome activation. RESULTS:(1) In vitro, in contrast to the control group, PA intervention caused increased ROS accumulation, reduced MMP, upregulated NLRP3 and caspase-1 expression, as well as elevated expression of inflammatory factors IL-1β and IL-6. The expression of nephrin and podocin was notably reduced. By contrast, NAC reversed these effects. (2) In vivo, JQHF effectively ameliorated mitochondrial damage, reduced NLRP3 expression and mitigated podocyte injury in PHN rats. The protective effects of JQHF were diminished by 3-MA, confirming the involvement of autophagy. (3) In vitro, JQHF-containing serum attenuated C5b-9-induced podocyte injury, improved mitochondrial dysfunction, and inhibited ROS-mediated activation of NLRP3 inflammasome. Silencing PINK1 significantly reversed these protective effects. CONCLUSION:JQHF can alleviate podocyte damage, that through inhibiting ROS-mediated NLRP3 inflammasome activation by improving PINK1-mediated mitophagy.

Ethnopharmacological relevanceMoshen Fuyuan Formula (MSFY) is one of the representative Chinese medicine compound for Idiopathic membranous nephropathy (IMN), that originate from Fang Ji Huang Qi decoction in the Han dynasty. IMN is usually accompanied by different tongue coatings in traditional Chinese medicine (TCM), and tongue microorganisms are important factors affecting the formation of the tongue coating. Recently, oral microbiomes, including bacteria and fungi, have been identified as pivotal factors that contribute to disease development. However, the regulation of oral microbiomes by MSFY has not been defined.Aim of the studyIn this work, we explore the characteristics of oral bacteria and fungi in IMN patients with different tongue coatings, and clarify the therapeutic effect of MSFY based on oral microbiome.Materials and MethodsWe enrolled 24 patients with IMN, including 11 with white tongue (IMN-W) and 13 with yellow tongue (IMN-Y), and recruited an additional 10 healthy individuals. Patients with IMN were treated with the MSFY. The oral bacteriome and fungi before and after treatment were detected using full-length 16S rRNA and internal transcribed spacer gene sequencing.ResultsThe therapeutic effect of MSFY on patients with yellow tongue coating was more significant than that on patients with white tongue coating. In terms of oral bacteriome, Campylobacter bacteria were enriched in patients with yellow tongue and could be a promising biomarker for yellow coating. Enrichment of Veillonella parvula_A may partially account for the therapeutic effect of MSFY. As for oral fungi, Malassezia globosa was enhanced in patients with IMN-W and reduced in patients with IMN-Y. Notably, it was reduced by MSFY. We also found that mycobiome-bacteriome interactions were highly complex and dynamic in patients with IMN.ConclusionThe regulation of the dynamic balance between oral fungi and bacteria by MSFY contributes to the treatment of IMN. This study determined the oral bacteriome and mycobiome of patients with IMN with different tongue coatings before and after MSFY treatment, which aids in promoting personalized treatment in clinical TCM and provides direction for investigating the mechanism of Chinese herbal medicines.

Professor NIE Lifang believes that the occurrence of chronic kidney disease is closely related to the spleen and the stomach dysfunction.In clinical practice,she flexibly applies eight methods of regulating the spleen and the stomach to treat chronic kidney disease based on different main symptoms or pathological mechanisms,namely,the method of harmonizing the stomach and lowering the adverse qi to stop vomiting,the method of invigorating the spleen to remove dampness and promote diuresis,the method of invigorating the spleen to benefiting qi and raise clear yang,the method of clearing heat and dampness in the middle jiao,the method of clearing stomach fire and promoting bowel movement,the method of tonifying both qi and yin of the spleen and the kidney,the method of invigorating the spleen and tonifying the kidney to warm yang,and the method of regulating the liver and the spleen to harmonize blood.Professor NIE emphasizes that when using the eight methods to regulate the spleen and the stomach,attention should be paid to whether the focus is on treating the spleen or treating the stomach.She advocates invigorating the spleen and benefiting qi,supplemented with medicinals that promote qi circulation and digestion to achieve the effect of tonifying without stagnation.Mean-while,She pays attention to the interrelationships of generation and restriction among the zang-fu organs,and particularly emphasizes the methods of decoc-tion and administration of medication.She believes that considering all aspects of diagnosis and treatment is essential for achieving good therapeutic effects.

Diabetic kidney disease(DKD)is a prevalent and severe microvascular complication of type 2 diabetes mellitus(T2DM).Chronic microinflammation is an important factor exacerbating renal tissue damage in DKD individuals.Macrophages play a crucial role in immune-inflammatory responses,and they can transiently and reversibly polarize into the pro-inflammatory M1 phenotype and anti-inflammatory M2 phenotype based on microenvironmental differences.The imbalance in M1/M2 macrophage polarization can exacerbate DKD progression by fostering inflammatory cytokine aggregation in the glomeruli and renal interstitium.Therefore,restoring the balance of macrophage is a pivotal avenue to ameliorate the chronic microinflammation state in DKD.Macrophage polarization is a complex and dynamic process.Various information molecules and cytokines involved in the polarization process play important roles in regulating phenotypes during the progression of DKD.They are closely related to various mechanisms such as metabolism,inflammation,fibrosis,and mitochondrial autophagy in DKD.By coordinating the inflammatory responses through polarization,they play a key role in regulating inflammation in metabolic-related diseases.The complex network of pathways involved in macrophage polarization corresponds well with the multi-pathway,multi-target treatment model of traditional Chinese medicine(TCM).Active ingredients and formulas of TCM can intervene in DKD by regulating macrophage polarization.Studies on relieving renal inflammation,repairing renal tissues,and promoting renal function recovery through macrophage polarization modulation are not uncommon.Therefore,based on exis-ting evidence,this study reviews TCM in targeting M1/M2 macrophage polarization balance to improve DKD,aiming to explore the potential of macrophage polarization in regulating DKD,which is expected to provide evidence support for the clinical diagnosis and treatment of DKD with TCM as well as the exploration of its biological mechanisms.

This study aimed to evaluate the efficacy of Qi-supplementing and Yin-nourishing Chinese patent medicine in the treatment of early diabetic nephropathy(DN) by network Meta-analysis to explore the Chinese patent medicine with optimal efficacy and provide references for preventing renal deterioration and delaying the progression of early DN. Eight databases, including CNKI, Wanfang, VIP, SinoMed, PubMed, EMbase, Cochrane Library, and Web of Science, were searched for clinical randomized controlled trial(RCT) of Qi-supplementing and Yin-nourishing Chinese patent medicines in the treatment of early DN. After the literature mee-ting the inclusion criteria was screened, the quality of the literature was evaluated using the Cochrane risk-of-bias tool, and network Meta-analysis was performed using the BUGSnet package in R 4.2.1. Seventy-two research articles with a sample size of 6 344 cases were included, involving eight Chinese patent medicines and seven outcome indicators. The results of the network Meta-analysis showed that(1)in terms of improving urinary albumin excretion rate(UAER), Chinese patent medicines combined with conventional treatment were superior to conventional treatment, and Qiyao Xiaoke Capsules + conventional treatment was optimal.(2)In terms of reducing serum crea-tinine(Scr), Bailing Capsules + conventional treatment had superior efficacy.(3)In terms of reducing 24-hour urine total protein(24hUTP), Shenyan Kangfu Tablets + conventional treatment and Jinshuibao Capsules + conventional treatment had equivalent efficacy, and Shenyan Kangfu Tablets + conventional treatment was superior.(4)In terms of improving fasting blood glucose(FBG), Shenyan Kangfu Tablets + conventional treatment had superior efficacy.(5)In terms of improving total cholesterol(TC), Qiyao Xiaoke Capsules +conventional treatment had superior efficacy.(6)In terms of reducing triglyceride(TG), Bailing Capsules + conventional treatment had superior efficacy.(7)In terms of safety, the occurrence of adverse reactions was reported in seven interventions, but due to the large clinical heterogeneity, the quantitative analysis could not be performed. Overall, Qi-supplementing and Yin-nourishing Chinese patent medicines combined with conventional treatment were superior to conventional treatment alone in the treatment of early DN. The results showed that Qi-supplementing and Yin-nourishing Chinese patent medicines combined with conventional treatment had good clinical efficacy, and they could significantly reduce renal function indicators such as UAER, Scr, and 24hUTP, and reduce blood sugar and blood lipid, which can provide evidence-based support for the treatment of early DN. However, due to the differences in the quantity and quality of the included research articles, large-sample, multi-center, high-quality studies are still needed for further verification.

Objective:To analyze the medication and compatibility law of TCM compound patents in the treatment of diabetic nephropathy (DN) based on data mining method; To provide basis for research and development of new drug in clinic.Methods:TCM compound patents for DN treatment were retrieved from national patent platform. Excel 2019 was used to conduct statistical analysis on drug frequency, property and taste and meridian. SPSS Modeler 18.0 and SPSS Statistic 26.0 were used for drug association rules and clustering analysis. The complex network of co-occurrence of core drugs was constructed with Cytoscape 3.9.0, and the potential of the correlation between new prescriptions and drugs was demonstrated.Results:A total of 261 TCM compound patents were included, including 438 kinds of Chinese materia medica. High-frequency drugs included Astragali Radix, Rehmanniae Radix, Salviae Miltiorrhizae Radix et Rhizoma, Lycii Fructus, etc. Drug categories were mainly deficiency tonic drugs. The properties and tastes were mainly cold and sweet, and the meridians were mainly liver and kidney meridians. The commonly used medicinal pair was Ganoderma-Rehmannine Radix. The commonly used triple medicinal combination was Notoginseng Radix et Rhizoma-Angelicae Sinensis Radix-Ganoderma. There were 7 groups of clustering medicines, including Notoginseng Radix et Rhizoma, Ganoderma, Angelicae Sinensis Radix, Euryales Semen, Rehmanniae Radix and Lycii Fructus. There were 5 groups of potential medicines, including Campsis Flos-Caulis Tinosporae Sinensis-Kalopanacis Radix-Fimbristylis Rigiduta Nees-Padicularisdis Dissectae Radix -Korshinsk Peashrub-Alismatis Fructus-Cynanchi Wallichii Radix. The core new prescriptions for treating DN were obtained through topological attribute analysis and screening.Conclusions:The national TCM compounds patents treatment for DN is based on the pathogenesis of this disease, which is characterized by deficiency in nature and excess in superficiality. It often uses methods such as tonifying qi and spleen, nourishing yin and tonifying kidney, promoting blood circulation and resolving blood stasis to improve clinical efficacy, providing ideas for the development of new drugs.

特发性膜性肾病是一种常见的原发性自身免疫性肾小球疾病,本病从脾论治不仅有中医理论渊源,且"脾"与人体的免疫功能密切相关.脾虚不仅涉及人体细胞免疫和体液免疫的紊乱,而且属于"脾"的肠道菌群也影响宿主的免疫稳态.中国中医科学医院西苑医院肾病科主任余仁欢教授经过多年临床实践,依据李东垣的"阴火论"提出脾虚是特发性膜性肾病的基本病机,脾虚不仅生湿,而且以脾胃为中心的中焦气机升降失常,会进而导致三焦气机郁滞,气滞血瘀,气郁化火,变证丛生,从而在脾虚或脾肾两虚基础上,常可兼夹风湿、湿瘀互结、或痰瘀互结.采用健脾益气、疏风散火、祛湿和络法治疗特发性膜性肾病,临床疗效显著,患者尿蛋白明显减少,不良反应少,生活质量明显改善.该文旨在详细阐述余仁欢教授从脾论治特发性膜性肾病的理论依据及临证经验,并验案一则加以佐证.

目的 探讨慢性肾脏病(CKD)3～5期非透析住院患者血钾与中医证型的相关性.方法 采用横断面调查,共纳入2018年10月—2021年10月在中国中医科学院西苑医院肾病科住院的CKD 3～5期非透析患者308例,采集患者一般资料、实验室指标及中医证型,分析中医证型与肾小球滤过率(eGFR)、CKD分期、血钾水平、高钾血症发生率的相关性.结果 因风动证及热毒证比例极少,故未纳入分析,纳入分析的患者298例.虚证中,脾肾气虚证70例、肝肾阴虚证41例、脾肾阳虚证57例、气阴两虚证93例、阴阳两虚证37例;阴阳两虚证患者eGFR和CKD3期所占比例均明显低于其他证型者(P均<0.05).脾肾气虚证和肝肾阴虚证患者血钾水平和高钾血症发生率均明显低于其他证型者(P均<0.05);阴阳两虚证患者血钾水平和高钾血症发生率均明显高于其他证型组(P均<0.05).兼实证情况中,无兼证28例,兼实证270例,其中湿浊证53例、湿热证45例、瘀血证43例、湿浊+瘀血证60例、湿热+瘀血证69例;不同兼实证情况之间eGFR及CKD分期比例差异均无统计学意义(P均>0.05);湿浊+瘀血证和湿热+瘀血证患者血钾水平和高钾血症发生率均明显高于无兼证者(P均<0.05);湿热证和血瘀证患者血钾水平明显高于无兼证者(P均<0.05).结论 血钾水平和高钾血症发生率与中医证型具有相关性,其中阴阳两虚证、兼湿热+瘀血证和兼湿浊+瘀血证患者血钾水平和高钾血症发生率更高,可能是受患者eGFR、胃肠功能和凝血功能因素影响所致,中医证型对于CKD早期预防高钾血症具有重要意义.

BACKGROUND The recognition of idiopathic membranous nephropathy (IMN) as an autoimmune disease has paved the way for the use of B-cell-depleting agents, such as Rituximab (RTX), which is now a first-line drug for treating IMN with proven safety and efficacy. Nevertheless, the usage of RTX for the treatment of refractory IMN remains controversial and challenging. AIM To evaluate the efficacy and safety of a new low-dose RTX regimen for the treatment of patients with refractory IMN. METHODS A retrospective study was performed on refractory IMN patients that accepted a low-dose RTX regimen (RTX, 200 mg, once a month for five months) in the Xiyuan Hospital of Chinese Academy of Chinese Medical Sciences’ Department of Nephrology from October 2019 to December 2021. To assess the clinical and immune remission data, we performed a 24 h urinary protein quantification (UTP) test and measured the serum albumin (ALB) and serum creatinine (SCr) levels, phospholipase A2 receptor (PLA2R) antibody titer, and CD19+ B-cell count every three months. RESULTS A total of nine refractory IMN patients were analyzed. During follow-up conducted twelve months later, the results from the 24 h UTP decreased from baseline [8.14 ± 6.05 g/d to 1.24 ± 1.34 g/d (P < 0.05)] and the ALB levels increased from baseline [28.06 ± 8.42 g/L to 40.93 ± 5.85 g/L (P < 0.01)]. Notably, after administering RTX for six months, the SCr decreased from 78.13 ± 16.49 μmol/L to 109.67 ± 40.87 μmol/L (P < 0.05). All of the nine patients were positive for serum anti-PLA2R at the beginning, and four patients had normal anti-PLA2R titer levels at six months. The level of CD19+ B-cells decreased to 0 at three months, and CD19+ B-cell count remained at 0 up until six months of follow-up. CONCLUSION Our low-dose RTX regimen appears to be a promising treatment strategy for refractory IMN.

ObjectivesGalactose-deficient IgA1 (Gd-IgA1) is a critical effector molecule in the pathogenesis of IgA nephropathy (IgAN), a leading renal disease without noninvasive assessment options. This updated systematic review aimed to determine the diagnostic and prognostic value of Gd-IgA1 assessment in biological fluids in patients with IgAN.MethodsPRISMA guidelines were followed in this review. We searched PubMed, Embase, Cochrane Library, China National Knowledge Infrastructure, China Biology Medicine disc, VIP Information/China Science and Technology Journal Database, and WANFANG for studies published between database inception and January 31, 2023. Eligible studies that evaluated aberrant IgA1 glycosylation in IgAN patients relative to controls were identified, and random effects meta-analyses were used to compare Gd-IgA1 levels in different groups. The quality of the evidence was assessed using the Newcastle-Ottawa Scale. This study was registered on PROSPERO (CRD42022375246).FindingsOf the 2727 records identified, 50 were eligible and had available data. The mean Newcastle-Ottawa Scale score was 7.1 (range, 6–8). Data synthesis suggested that IgAN patients had higher levels of blood and/or urine Gd-IgA1 compared with healthy controls (standard mean difference [SMD]=1.43, 95% confidence interval [CI]=1.19−1.68, P<0.00001), IgA vasculitis patients (SMD=0.58, 95% CI=0.22−0.94, P=0.002), and other kidney disease patients (SMD=1.06, 95% CI=0.79−1.33, P<0.00001). Moreover, patients with IgAN had similar levels of serum Gd-IgA1 compared to first-degree relatives (SMD=0.38, 95% CI= -0.04−0.81, P=0.08) and IgA vasculitis with nephritis patients (SMD=0.12, 95% CI= -0.04−0.29, P=0.14). In addition, ten studies demonstrated significant differences in serum Gd-IgA1 levels in patients with mild and severe IgAN (SMD= -0.37, 95% CI= -0.64−-0.09, P=0.009).ConclusionsHigh serum and urine Gd-IgA1 levels suggest a diagnosis of IgAN and a poor prognosis for patients with this immunological disorder. Future studies should use more reliable and reproducible methods to determine Gd-IgA1 levels.Systematic review registrationhttps://www.crd.york.ac.uk/prospero/display_record.php?ID=CRD42022375246, identifier CRD42022375246.