The environmental factors underlying idiopathic membranous nephropathy (IMN) remain inadequately comprehended. Our purpose is to investigate the environmental factors that contribute to the IMN. Polycyclic aromatic hydrocarbons (PAHs) as a major harmful component of airborne particulate matter, are suspected to be associated with IMN. We employed a 1:1 pair-matched case-control, network toxicology and molecular docking to validate the role of urinary PAHs metabolites in IMN pathogenesis. Urine samples from 146 IMN patients and 146 controls were analyzed for six monohydroxylated PAHs using UPLC-MS/MS. The creatinine-adjusted 1-hydroxynaphthalene (1-OHNAP), 2-hydroxynaphthalene (2-OHNAP), total hydroxynaphthalene (∑OHNAP), and total OHPAHs (∑OHPAHs) were significantly higher in IMN patients (P < 0.05) with odds ratios of 1.42, 1.66, 1.29, and 1.19 respectively, indicating a significantly increased risk of IMN. 8-OHdG were higher in the IMN group. Subgroup analyses indicated stronger associations among males and drinkers. The RCS curve shows that PAHs concentration increases, the risk of IMN generally rises. (P < 0.05). Integrated network toxicology and molecular docking identified TGFβ1 as a key potential target. Molecular dynamics simulations confirmed a stable binding interaction between 2-OHNAP and TGFβ1. This finding was further supported by external RNA-seq data showing elevated TGFβ1 expression in the glomeruli of IMN patients. We report novel evidence suggesting that exposure to PAHs may contribute to the risk of IMN by disrupting immune system, highlighting the environmental factors driving IMN and offering potential therapeutic targets for this increasingly prevalent glomerular disease.

N-(1,3-dimethylbutyl)-N-phenyl-p-phenylenediamine quinone (6PPD-Q), a quinone derivative of the tire antioxidant 6-PPD, has exhibited toxic effects across a wide range of organisms. However, its nephrotoxicity and underlying mechanisms in mammals remain largely unknown. Herein, we demonstrated the renal toxicity of 6PPD-Q using in vivo and in vitro models. Further analysis revealed that 6PPD-Q exposure triggered ferroptosis in podocytes, as characterized by elevated intracellular ROS and Fe2 + levels, downregulation of GPX4, and accumulation of lipid peroxidation. A genome-wide CRISPR/Cas9 knockout screen identified EXOC7 as a critical mediator of 6PPD-Q-induced podocyte injury. Mechanistically, 6PPD-Q disrupted the E3 ubiquitin ligase activity of MARCHF2, leading to reduced ubiquitination of EXOC7, subsequent attenuation of its proteasomal degradation, and consequent accumulation of EXOC7 protein, which ultimately promoted ferroptosis. Limited proteolysis-mass spectrometry (LIP-MS) further revealed that 6PPD-Q directly bound to EXOC7, interfering with its recognition and ubiquitination by MARCHF. Importantly, inhibition of EXOC7 or ferroptosis alleviated chronic 6PPD-Q-induced oxidative stress and podocyte injury in vivo. Together, these findings identify a previously unknown molecular mechanism for 6PPD-Q-induced nephrotoxicity and establish EXOC7-mediated ferroptosis as a sensitive mechanistic endpoint for assessing environmental 6PPD-Q exposure.

Background Impaired fatty acid oxidation (FAO) inducing lipotoxicity in renal tubules is key in diabetic kidney disease (DKD) progression, yet mechanisms are unclear. Metadherin (MTDH) is linked to DKD but its role in renal lipotoxicity is unknown. Method A DKD mouse model was established via unilateral nephrectomy, high-fat diet, and STZ. Palmitate acid-induced renal tubular epithelial cells were also used. Renal MTDH in mice was knocked down using AAV9, and MTDH was silenced or overexpressed in vitro. Result In mice, MTDH knockdown improved renal function, enhanced FAO via PPARα, and reduced lipid toxicity. In vitro, MTDH silencing mitigated lipid accumulation and activated FAO, while overexpression aggravated injury, reversed by PPARα agonist. Conclusion MTDH upregulation in diabetic kidney disrupts lipid homeostasis by repressing PPARα-mediated FAO, promoting lipotoxic injury, offering new insights into DKD metabolic dysregulation.

Disentangling the nonlinear and interactive effects of chemical mixtures remains a central challenge in environmental health, hindering etiologic understanding of immune-mediated diseases such as primary membranous nephropathy (PMN). We developed a multi-stage pipeline integrating exposure clustering, penalized feature selection, interpretable machine learning, and model-based causal inference framework to dissect metal impacts on immune-renal dysfunction. Among 795 adults in Guangxi, China, we quantified 21 plasma metals and three endpoints: PMN diagnosis, estimated glomerular filtration rate (eGFR), and uric acid. Clustering revealed Zn-dominant profiles enriched in PMN patients versus Fe-centered patterns in controls. Tree-based models with SHAP interpretation identified Ba and Tl as being positively associated with PMN, while Co and Ni showed inverse associations. Mo was further linked to elevated uric acid and reduced eGFR, indicating coordinated relationships across metabolic and renal biomarkers rather than definitive evidence of toxicity. Interaction analyses revealed complex, nonlinear relationships, including NiCu antagonism and CoNi dose-modulated associations, highlighting the collective dynamics of metal mixtures in influencing PMN risk. As the first study to couple plasma metal exposomics with interpretable and causal-inspired machine learning in PMN, this work identifies novel exposure patterns and generates etiologic hypotheses, offering a transferable analytic framework for environmental health research.

AbstractBackground: Primary membranous nephropathy (PMN) is hypothesized to result from interactions between genetic susceptibility, particularly polymorphisms in the phospholipase A2 receptor 1 (PLA2R1) gene, and environmental factors. However, the joint effects of metal exposure and PLA2R1 variants on PMN risk remain largely unknown.Methods: This hospital-based case-control study enrolled 125 PMN patients and 375 healthy controls. Plasma levels of 16 metals were measured via inductively coupled plasma mass spectrometry (ICP-MS). Eight functional single nucleotide polymorphisms (SNPs) in the PLA2R1 gene (rs16844715, rs2715918, rs1511223, rs3749117, rs3749119, rs3828323, rs4664308, and rs4665143) were genotyped by Sanger sequencing. Associations and interactions were analyzed using logistic regression, weighted quantile sum (WQS) regression, extreme gradient boosting (XGBoost), the least absolute shrinkage and selection operator (LASSO), and multiplicative and additive interaction models.Results: After adjusting for confounders, higher plasma levels of vanadium (V), manganese (Mn), zinc (Zn), arsenic (As), strontium (Sr), molybdenum (Mo), cadmium (Cd), tungsten (W), thallium (Tl), and lead (Pb) were associated with increased risk of PMN, whereas cobalt (Co), nickel (Ni), selenium (Se), and rubidium (Rb) were associated with decreased PMN risk (all P < 0.05). Multi-method screening identified Zn, Mo, Tl, and Ni as key metals associated with PMN. The PLA2R1 SNPs rs3749117 and rs3749119 were significantly associated with susceptibility to PMN (P < 0.05). And the rs3749117 polymorphism exhibited negative additive interactions with plasma Zn (relative excess risk due to interaction (RERI) = −12.59; 95% confidence interval (CI): −65.86 to −1.56) and Mo (RERI = −6.25; 95% CI: −33.60 to −0.44), as well as a negative multiplicative interaction with Ni (odds ratio (OR) = 0.10; 95% CI: 0.01–0.99) on PMN risk. The rs3749119 polymorphism also demonstrated a negative additive interaction with Mo (RERI = −18.46; 95% CI: −116.62 to −2.49) in modulating susceptibility to PMN.Conclusions: The development of PMN appears to result from the combined effects of environmental metal exposure and genetic susceptibility. PLA2R1 polymorphisms interact with Zn, Mo, and Ni exposure, collectively contributing to PMN pathogenesis.

Phthalates (PAEs), widely used in plastics and consumer products, have raised growing concern due to the potential adverse health effects of their metabolites. While several epidemiological studies have linked PAE metabolites to nephrotoxicity, most have focused on exposure-response associations, leaving their molecular targets and mechanisms insufficiently defined. Here, we observed that mono-2-ethylhexyl phthalate (MEHP) was associated with reduced estimated glomerular filtration rate (eGFR) (WQS weight = 0.31) and increased albuminuria (WQS weight = 0.15) in patients with chronic kidney disease (CKD). In vivo, MEHP exposure preferentially induced glomerular injury, characterized by foot process effacement, while renal tubules remained unaffected. A genome-wide CRISPR-Cas9 screen highlighted toll-like receptor 4 (TLR4) as a potential mediator of MEHP-induced podocyte damage via MyD88-JNK pathway activation. In vitro experiments demonstrated that TLR4 activation by MEHP triggered downstream MyD88 recruitment and JNK phosphorylation, leading to podocyte injury. Notably, MEHP did not change TLR4 expression levels but directly interacted with TLR4 at Glu439 and MD2 at Arg90, promoting dimerization of the TLR4-MD2 complex and subsequent JNK activation. Furthermore, inhibition or genetic deletion of TLR4 mitigated MEHP-related nephrotoxic responses in acute kidney injury and CKD models. These findings suggest a TLR4-dependent mechanism that may contribute to MEHP-associated kidney effects, supporting the importance of continued efforts to reduce PAE exposure.

PURPOSE:Mitochondrial dysfunction leading to impaired energy metabolism has been recognized as a pivotal factor contributing to renal tubular epithelial cells (RTECs) damage in the context of dyslipidemia conditions in diabetic kidney disease (DKD). The primary objective of this study is to elucidate the role and underlying mechanism of the proto-oncogene Metadherin (MTDH) in mediating mitochondrial damage within this specific pathological context in vitro. METHODS:The expression of MTDH in RTECs was modulated by transfecting small interfering RNA and plasmid, while palmitic acid (PA) was employed to simulate diabetic lipid metabolism disorder. Mitochondrial damage was evaluated by examining various parameters including mitochondrial morphology, membrane potential, reactive oxygen species (ROS) production, adenosine triphosphate (ATP) production, as well as morphological and structural alterations. Additionally, Carnitine acetyltransferase (CrAT) expression was assessed using Western blotting and quantitative real-time polymerase chain reaction, and CrAT activity was quantified. RESULT:MTDH expression was upregulated in PA-induced RTECs, while CrAT expression and activity were inhibited. Downregulation of MTDH mitigated PA-induced mitochondrial damage, as demonstrated by the preservation of mitochondrial membrane potential, reduction in mitochondrial ROS production, prevention of ATP depletion, and maintenance of mitochondrial structure. This was accompanied by an upregulation in CrAT expression and activity. Conversely, overexpression of MTDH exacerbated mitochondrial dysfunction by impairing membrane potential, augmenting mitochondrial ROS production, inhibiting ATP synthesis, and suppressing CrAT expression and activity. CONCLUSION:In the context of dyslipidemia conditions, MTDH is upregulated and suppresses the expression and activity of CrAT in RTECs, thereby inducing mitochondrial dysfunction and perturbing energy metabolism. These alterations exacerbate the injury to RTECs, consequently promoting the progression of DKD.

Manganese (Mn) is an essential micronutrient required for various biological processes but excess exposure to Mn can cause neurotoxicity. However, there are few reports regarding the toxicity effect of Mn on the kidney as well as the underlying molecule mechanism. Herein, in vivo experiments were adopted to assess the toxicity effects associated with Mn, and found that chronic Mn treatment induced the injury of glomerular podocytes but not renal tubule in rats. Genome-wide CRISPR/Cas9 knockout screen was then employed to explore the biotargets of the toxic effect of Mn on podocytes. Through functional analyses of the enriched candidate genes, NLRP10 was found to be significantly up-regulated and mediated Mn-induced podocyte apoptosis. Further mechanism investigation revealed that NLRP10 expression was regulated by demethylase AlkB homolog 5 (ALKBH5) in an m6A-dependent fashion upon Mn treatment. Moreover, Mn could directly bind to Metadherin (MTDH) and promoted its combination with ALKBH5 to promote NLRP10 expression and cell apoptosis. Finally, logistic regressions, restricted cubic spline regressions and uniform cubic B-spline were used to investigate the association between Mn exposure and the risk of chronic kidney disease (CKD). A U-shaped nonlinear relationship between CKD risk and plasma Mn level, and a positive linear relationship between CKD risk and urinary Mn levels was found in our case-control study. To sum up, our findings illustrated that m6A-dependent NLRP10 regulation is indispensable for podocyte apoptosis and nephrotoxicity induced by Mn, providing fresh insight into understanding the health risk of Mn and a novel target for preventing renal injury in Mn-intoxicated patients.

Objective To explore the effects of polycyclic aromatic hydrocarbons（PAHs） exposure and its interaction with alcohol consumption on the mental health of non-smokers. Methods A questionnaire survey and mental health assessment were conducted among 513 non-active smokers in a large enterprise in Guangxi. The general mental health questionnaire was used to evaluate the mental health status of the subjects. Urinary hydroxypolycyclic aromatic hydrocarbons（OH-PAHs） levels were employed as an indicator of internal exposure to PAHs. Logistic regression model and generalized linear model were employed to analyze effects of PAHs exposure and its interaction with alcohol consumption on mental health status. Results The average age of the subjects in this study was（39.60±6.60） years old. 44.2% of the subjects were drinkers, with most being unmarried, male, and exposed to secondhand smoke（P＜0.05）. Logistic regression analysis showed that the increase of urine concentration of 1-hydroxynaphthalene（1-OHNAP） and total hydroxynaphthalene（∑OHNAPs） was associated with the risk of poor mental health（OR=1.23, 95% CI: 1.01-1.49; OR=1.10, 95% CI: 1.00-1.21; all P＜0.05）. Interaction analysis showed that compared with non-drinking and low level OH-PAHs group, the concentration of 1-OHNAP, 2-hydroxynaphthalene（2-OHNAP）, ∑OHNAPs and total hydroxypolycyclic aromatic hydrocarbons（∑OHPAHs） in urine and alcohol consumption increased the risk of poor meatal health in middle-aged and older adults(OR=3.91, 95% CI:1.01-15.11; OR=3.69, 95% CI: 1.05-12.98; OR=1.96, 95% CI: 1.01-3.80; OR=1.73, 95% CI: 1.06-2.93; all P int ＜0.05). Conclusions PAHs exposure is a risk factor for poor mental health in non-smoking populations, and alcohol consumption can exacerbate the risk of poor mental health in middle-aged and elderly non-smokers exposed to PAHs.

Immunoglobulin A nephropathy (IgAN) is the most common type of glomerulonephritis in adults worldwide. Environmental metal exposure has been reported to be involved in the pathogenic mechanisms of kidney diseases, yet no further epidemiological study has been conducted to assess the effects of metal mixture exposure on IgAN risk. In this study, we conducted a matched case‒control design with three controls for each patient to investigate the association between metal mixture exposure and IgAN risk. A total of 160 IgAN patients and 480 healthy controls were matched for age and sex. Plasma levels of arsenic, lead, chromium, manganese, cobalt, copper, zinc, and vanadium were measured using inductively coupled plasma mass spectrometry. We used a conditional logistic regression model to assess the association between individual metals and IgAN risk, and a weighted quantile sum (WQS) regression model to analyze the effects of metal mixtures on IgAN risk. Restricted cubic splines were used to evaluate overall associations between plasma metal concentrations and estimated glomerular filtration rate (eGFR) levels. We observed that except for Cu, all the metals analyzed were nonlinearly associated with decreased eGFR, and higher concentrations of arsenic and lead were associated with elevated IgAN risk in both single-metal [3.29 (1.94, 5.57), 6.10 (3.39, 11.0), respectively] and multiple-metal [3.04 (1.66, 5.57), 4.70 (2.47, 8.97), respectively] models. Elevated manganese [1.76 (1.09, 2.83)] levels were associated with increased IgAN risk in the single-metal model. Copper was inversely related to IgAN risk in both single-metal [0.392 (0.238, 0.645)] and multiple-metal [0.357 (0.200, 0.638)] models. The WQS indices in both positive [2.04 (1.68, 2.47)] and negative [0.717 (0.603, 0.852)] directions were associated with IgAN risk. Lead, arsenic, and vanadium contributed significant weights (0.594, 0.195, and 0.191, respectively) in the positive direction; copper, cobalt, and chromium carried significant weights (0.538, 0.253, and 0.209, respectively). In conclusion, metal exposure was related to IgAN risk. Lead, arsenic, and copper were all significantly weighted factors of IgAN development, which may require further investigation.

Pulmonary rehabilitation（PR） is based on a comprehensive assessment of patients with respiratory diseases and lung surgery, so that patients can be customized for their own individualized comprehensive intervention and treatment programs. PR is not only limited to exercise training, but also includes health education, nutritional support and psychological intervention. PR is a continuation of clinical treatment and an important preventive measure for respiratory diseases. The diaphragm is the most important respiratory muscle in the human body. It participates in about 80% of the respiratory process and is the main power source of respiratory movement. In addition to participating in respiratory movement, it also participates in the completion of human expectoration, defecation, delivery, vomiting and other movements. Therefore, the reference to PR is essential to pay attention to diaphragmatic function. The main purpose of PR is to relieve or control the acute symptoms and complications of respiratory diseases, improve their endurance of exercise and activity, shorten hospitalization time or reduce the need for hospitalization. In addition, we should try to eliminate the dysfunction and psychological effects left by the disease, and give full play to their own respiratory potential through active breathing and exercise training. Therefore, it is particularly important to evaluate PR as early as possible and actively intervene. Based on this, this article mainly reviews the evaluation methods of PR and the progress of PR in clinical application.

目的:探讨成人原发性膜性肾病原发性膜性肾病(PMN)伴乙肝病毒(HBV)感染的临床特点及预后.方法:回顾性分析2015年1月至2020年10月在广西医科大学第一附属医院肾内科住院治疗并经肾活检确诊的成人PMN患者临床资料,比较伴或不伴HBV感染的PMN患者的临床特点,运用Kaplan-Meier生存分析和COX回归分析比较两组患者的预后.结果:共纳入PMN患者88例,其中伴HBV感染(PMN-HBV组)49例,不伴HBV感染(PMN组)39例;PMN-HBV组谷草转氨酶(AST)、谷丙转氨酶(ALT)、24h尿蛋白水平高于PMN组(P＜0.05),而补体C3、C4水平低于PMN组(P＜0.05).两组间在其他临床指标及药物使用上差异均无统计学意义(P＞0.05).Kaplan-Meier生存分析显示,PMN组临床缓解率高于PMN-HBV组(Log-rank x2=5.124,P=0.024).多因素COX回归分析显示,合并HBV感染是影响PMN临床缓解的影响因素(HR=0.049,95％CI=0.214～0.899,P=0.024).结论:伴HBV感染是影响成人PMN患者临床缓解的影响因素,伴HBV感染的成人PMN患者预后较差.

目的:分析多发性肺结节患者的病理学特征与临床流行病学,了解多发肺结节流行趋势,提高疾病筛查率,以期为临床提供参考.方法:回顾性分析2018年8月～2020年8月于广东医科大学附属医院胸外科就诊的248例多发性肺结节患者的病理学特征以及临床流行病学资料.结果:在248例多发性肺结节患者中,多发性结节患者不同年龄段差异有统计学意义.男女性多发性结节患者均以腺癌为主.男性患者的良性肿瘤比例高于女性患者.有吸烟史多发性结节患者中腺癌所占比例较高.不同性别多发性结节患者在吸烟史比较上存在差异,女性不吸烟患者多见.高龄为多发性肺结节原发恶性肿瘤的独立危险因素.结论:多发性肺结节在中老年高发,多见于女性、无吸烟史患者.病理类型以腺癌为主,尤其女性多发性结节患者以腺癌为高发类型.随着年龄增长,多发性肺结节腺癌比例呈上升趋势,良性结节比例呈下降趋势.

目的:探讨同型半胱氨酸（homocysteine，Hcy）早期预测IgA肾病（IgA nephropathy，IgAN）肾脏预后不良的临床价值。方法:回顾性分析广西医科大学第一附属医院原发性IgAN患者的临床资料，依据血Hcy水平将患者分为高Hcy组（Hcy>15 μmol/L）和Hcy正常组（Hcy≤15 μmol/L），比较两组患者间临床病理指标的差异。采用Cox回归模型法分析肾脏预后不良的危险因素。Kaplan-Meier生存曲线和Log-rank检验比较两组患者肾脏累积生存率的差异。结果:196例IgAN患者入选，男女比为1.15∶1，年龄（37.01±10.95）岁。高Hcy组62例（31.6%），Hcy正常组134例（68.4%）。与Hcy正常组比较，高Hcy组患者男性比例、收缩压、血白蛋白、血肌酐及血尿酸水平均较高，高密度脂蛋白胆固醇和估算肾小球滤过率均较低，肾小管萎缩/间质纤维化程度较严重，细胞/纤维细胞性新月体比例较高（均 P<0.05）。Cox回归分析结果显示，随访（30.0±16.0）个月，基线高Hcy血症是IgAN肾脏预后不良的独立危险因素（ HR=10.002，95% CI 2.019~49.555， P=0.005）。Kaplan-Meier生存曲线分析结果显示，高Hcy组患者累积肾脏生存率明显低于Hcy正常组（Log-rank检验 χ2=18.971， P<0.001）。 结论:Hcy是IgAN肾功能进展的影响因素，高血Hcy水平可作为预测IgAN肾脏预后不良的影响因素之一。

膈肌是人体中最主要的呼吸肌,除协助呼吸外,还与腹肌共同参与人体排便、排尿、分娩、呕吐等动作的完成.手术、麻醉、呼吸机的使用等带来的医源性伤害,以及膈肌本身的一些原发性和继发性疾病诱发的损伤会影响膈肌的功能,导致患者术后肺部并发症发生、术后呼吸困难、脱机困难等.在膈肌功能测定中,经膈神经磁刺激所诱发出的颤搐性跨膈压被认为是客观评估膈肌强度的金标准.但跨膈压的测定需留置胃-食道囊管,从而影响了其临床应用.超声由于具有无创、床旁实时动态观察、安全方便等优势,在临床应用中优于跨膈压测定、膈肌肌电图、放射学检查等方法.膈肌超声指标包括膈肌移动度、膈肌厚度、膈肌增厚率(DTF)、膈肌收缩速度、膈肌偏移-时间指数、膈肌浅快呼吸指数(D-RSBI)、膈肌增厚浅快呼吸指数(DT-RSBI)、膈肌对合角度、剪切波弹性成像(SWE)等.目前膈肌超声主要应用于指导机械通气撤机拔管时机、诊断慢性阻塞性肺疾病(COPD)、预测术后恢复及指导康复治疗等.基于此,本文对膈肌功能测定及近年来膈肌超声评估的进展进行综述.

Household animal fat has been linked to increased incidence of cancers compared with vegetable fat. However, few epidemiological studies have associated these two cooking oil types with precancerous genotoxic effects, such as occurrence of micronuclei (MN). This study aimed to explore the association between oral MN frequency and household cooking oil type and whether the association can be attributed to polycyclic aromatic hydrocarbons (PAHs). We collected information about individual cooking oil use, measured genotoxic effects by MN tests and urinary PAHs metabolites (OHPAHs) in 245 nonsmokers. The associations between household cooking oil type and MN frequency and OHPAHs were analyzed using generalized linear models (GLMs) and logistic regression models, evaluating odds ratios and coefficient (95% confidence intervals) (ORs, 95% Cls; β, 95% Cls). The odds of animal fat consumers, rather than vegetable fat consumers, was positively associated with higher MN frequency (OR = 1.94, P < 0.05). The associations were discovered in participants only using kitchen ventilation (OR = 2.04, P < 0.05). Animal fat consumers had higher total OHPAHs than vegetable fat consumers (1.58 ± 0.22 mg/mol, Cr vs 1.20 ± 0.12 mg/mol, Cr; P = 0.028). Significant correlations were observed between total OHPAHs quartiles and increased MN frequency (β = 0.38, P-trend = 0.026). After stratifying by household cooking oil type, sensitivity analyses showed that the positive association between total OHPAHs quartiles and increased MN frequency was only observed in animal fat consumers (β = 0.61, P-trend = 0.030). In conclusion, usage of household animal fat was associated with an increased odds of oral MN frequency in Chinese nonsmokers and the odds correlated with increased PAHs exposure. This finding supplemented evidence associating cooking oil type with genotoxic effects and explained its association with PAHs exposure.

目的 研究伴足突融合的IgA肾病(IgAN)患者的临床病理特征,探讨足突融合对IgA肾病患者肾功能的影响.方法 回顾性分析我院219例IgA肾病患者资料,根据电镜下足突病变分为足突广泛融合组(融合≥50％)40例(18.3％)和足突无明显病变组(包括无病变和<50％融合)179例(81.7％).结果 足突广泛融合组与无明显病变组比较,血肌酐、尿素氮、尿酸、舒张压、胆固醇、甘油三酯、低密度脂蛋白(LDL)及尿蛋白定量更高,血白蛋白及肾小球滤过率估值(eGFR)更低.舒张压、尿素氮及LDL升高是足突广泛融合的独立危险因素.logistic结果显示足突广泛融合是IgA肾病肾功能异常的独立危险因素(P<0.05).结论 足突广泛融合的IgAN患者临床表现更重,足突广泛融合是IgA肾病患者肾功能的重要影响因素.

目的 研究影响原发性膜性肾病(primary membranous nephropathy,PMN)治疗后复发的危险因素,以期寻找出初治的PMN 患者有预后预测意义的指标,能够早期发现高危因素的患者,减少PMN 患者的复发,降低进展至终末期肾病的可能性.方法 选取2012年1 月至2020年5 月在我院经肾穿病理活检确诊的初治的PMN 患者作为研究对象,按照疗效分为复发组和非复发组,分析和比较复发组和非复发组的相关临床资料.结果 PMN 患者复发多因素Cox 回归分析结果显示,高血压、高尿酸是PMN 复发的独立危险因素.结论 膜性肾病复发的主要危险因素为高血压、高尿酸血症,多发生在药物减量、停药和感染的情况下.

肺癌是我国最常见的恶性肿瘤之一,其中非小细胞肺癌(NSCLC)约占85％,且大部分NSCLC患者在确诊时疾病已进展至晚期,病死率较高.近年来,临床对于晚期NSCLC的治疗已从传统的手术治疗、化学治疗、放射治疗、靶向治疗走向了免疫治疗.免疫检查点抑制剂(ICIs)治疗晚期NSCLC体现出了良好的抗肿瘤活性,尤其体现在细胞毒性T淋巴细胞相关抗原-4(CTLA-4)、程序性死亡受体-1(PD-1)、程序性死亡配体-1(PD-L1)抑制剂.基于此,本文将重点综述CTLA-4、PD-1、PD-L1抑制剂在晚期NSCLC中的治疗进展,以期提高患者的临床获益率,为临床选择合理治疗方案提供参考.

Objective To analyze the clinical features of nutcracker syndrome complicated with IgA nephropathy, so as to improve the accuracy of diagnosis and efficiency of treatment. Methods Thirty cases of patients with nutcracker syndrome complicated with IgA nephropathy were designated as group I; 90 cases of adult patients with IgA nephropathy without nutcracker syndrome, who had undergone left renal vein Doppler examination, as group II; and 60 cases of patients with single nutcracker syndrome as group III. Clinical, laboratory, imaging and pathological data of patients in the three groups were analyzed retrospectively. Results The ratio of male to female in group I was 1∶3.29, which showed that females were significantly more than males. The body mass index in groupⅠand Ⅲ were lower than group Ⅱ. The hypo-C3-emia rate in group I was 56.7%, higher than that in group II(P<0.01). The inner diameter at the left renal vein site with stenosis with groupⅠand Ⅲ was evidently narrower than that with groupⅡ(P<0.01). Conclusions It’s recommended that, those adult patients with long-term nutcracker syndrome with hypo-C3-emia should undergo renal biopsy for a definitive diagnosis; and left renal vein Doppler ultrasonic examination should be taken into account for those slim female adults with IgA nephropathy with decreased serum C3 level.