IgA nephropathy (IgAN) is a common type of primary glomerulonephritis worldwide with nearly 40% of patient progresses to end-stage renal disease (ESRD) in 10-20 years. The most widely accepted hypothesis is known as the ‘multihit hypothesis’. B cells play an important role in producing galactose-deficient IgA1 (Gd-IgA1) and its autoimmune antibody, resulting in the deposition of IgA in the mesangium. B-cell activating factor (BAFF), also known as B-lymphocyte stimulator (BLyS), and a proliferation-inducing ligand (APRIL) have been reported to play crucial roles in the activation of B lymphocytes. Telitacicept, a soluble humanized recombinant fusion protein that effectively neutralizes the activity of BLyS and APRIL had been demonstrated the ability to reduce proteinuria with adverse events similar to supportive care in a phase 2 clinical trial. Therefore, our project was aiming to conduct a large single-center observational study to explore the efficacy and safety of telitacicept in patients with IgAN compared with supportive therapy and glucocorticoid therapy. We are aiming to conduct a observational study of adults who had undergone renal biopsy at the First Hospital of Jilin University between October 2023 and December 2026 and were diagnosed with IgAN. Up to now, out of the initial pool of 243 patients, 159 were excluded based on specific criteria: (1) eGFR (CKD-EPI) <35 mL/min/1.73 m² (n = 39); (2) proteinuria <0.5 g/d (n = 10); (3) others (n = 109). So far, 84 eligible IgAN patients were enrolled in the project and 64 IgAN patients can be analysed due to the fllowed-up time. All patients received supportive care and were taking the maximally tolerated dose of angiotensin receptor blockers. The patients were divided into four groups according to the therapy: telitacicept (Group A, not enough cases now), telitacicept combined low-dose corticosteroids (Group B, n = 20), adequate-dose of glucocorticoids (Group C, n = 21) and angiotensin receptor blockers (Group D, n = 23). The efficacy was defined as a decrease in proteinuria of 50% or more. The research protocol underwent thorough scrutiny and received approval from the ethical committees of the First Hospital of Jilin University (approval number: 2024-1165). A cohort of 64 patients with IgAN were recruited with a follow-up duration of 12 weeks. All the clinical data has no significance among Group B, C and D. The median baseline proteinuria of Group B, C, D was 1.85 g/day, 1.34 g/day and 1.26 g/day respectively, while median baseline eGFR was 62.98 mL/min/1.73 m2, 82.26 mL/min/1.73 m2 and 78.44 mL/min/1.73 m2. Patients with higher proteinuria and lower eGFR are more likely to choose telitacicept. Renal biopsy data showed significance in T classification. The total efficacy among the three group also has no significance. Figure 1 showed the changing process of proteinuria and eGFR at week 4, week 8 and week1, indicates that telitacicept combined low-dose corticosteroids can reduce proteinuria and stabilize eGFR in patients with IgAN. However the adequate-dose of glucocorticoids seemed to keep urine protein at a lower level than telitacicept within 12 weeks, the long follow-up of our project may give the answer later. Telitacicept can reduce the dose of corticosteroids and is no inferior to corticosteroid therapy in IgAN, the long-term kidney protection still needs to be confirmed.

Background Immunoglobulin A nephropathy (IgAN) patients with acute kidney injury (AKI) have an elevated risk of adverse events and mortality. However, there is currently a lack of convenient and effective clinical tools to predict AKI risk in this population. The present study was conducted to create such tools containing inflammatory and nutritional indexes. Method Data from 720 adults diagnosed with IgAN by renal biopsy at the First Hospital of Jilin University were collected. They were randomly divided into a training set (n = 503) and a test set (n = 217) in a 7:3 ratio. Univariate and multivariate logistic regression analyses with backward selection were used to identify risk factors, resulting in multiple prediction models. The least absolute shrinkage and selection operator (LASSO) regression was used to simplify the model. The models were presented using nomograms, and their performances were evaluated through receiver operating characteristic (ROC) curves, area under the curve (AUC), Hosmer-Lemeshow test, net reclassification improvement (NRI), integrated discrimination improvement (IDI), calibration curves, and clinical decision curve analysis (DCA). Results Eleven risk factors related to IgAN with AKI were identified, including nephrotic syndrome (NS), T score from the Oxford histological classification, estimated glomerular filtration rate (eGFR), blood urea nitrogen (BUN), 24-hour urinary protein quantification (24h-UPRO), C-reactive protein (CRP), systemic inflammatory response index (SIRI), lymphocyte-to-monocyte ratio (LMR), platelet-to-lymphocyte ratio (PLR), lymphocyte-to-CRP ratio (LCR), and prognostic nutritional index (PNI). These factors contributed to the development of seven prediction models. ROC curves indicated good predictive performance for all models, with the full model performing best. The Hosmer-Lemeshow test showed that six models fit well in the test set. DCA results demonstrated significant clinical benefits for all models. Conclusion CRP, SIRI, LMR, PLR, LCR, and PNI were identified as novel AKI predictors in patients with IgAN. A series of prediction models incorporating these factors were developed for better clinical applicability, with the full model performing the best.

BackgroundInflammation plays a crucial role in occurrence of kidney injury, and specific dietary patterns can influence systemic inflammation levels. However, the relationship between dietary inflammatory potential and early-stage kidney damage remains unclear.Method2,108 participants was recruited from 2001-2002 National Health and Nutrition Examination Survey (NHANES). Dietary Inflammatory Index (DII) is utilized to assess dietary inflammatory potential, calculated through a 24-h dietary recall questionnaire. Early renal injury was evaluated using urinary albumin to creatinine (UACR), cystatin C (CysC), beta-2 microglobulin (beta 2M), and estimated glomerular filtration rate (eGFR) based on serum creatinine (eGFRs), cystatin C (eGFRc), and both Scr and CysC (eGFRs&c). Participant characteristics were analyzed, and association between DII, hypertension, and early renal injury markers was explored using multiple linear and logistic regression models.ResultsThe average age of participants was 53.9 years. DII exhibited a positive correlation with UACR (beta = -0.048[0.017,0.078]), beta 2M (beta = 0.019[0.010,0.027]), CysC (beta = 0.012 [0.004,0.021]). Conversely, a negative correlation was observed between DII and eGFRc (beta = -1.126[-1.554, -0.699]), eGFRs&c (beta=-1.101[-1.653, -0.549]). A significant association was observed between hypertension and abnormality of early kidney damage markers. Subgroup analysis reveals that the positive correlation between DII and the occurrence of abnormal markers of early kidney damage is only observed in individuals with hypertension. Furthermore, an interaction between DII and hypertension was detected in eGFRs&c (OR:1.250[1.042, 1.499], p for interaction = 0.03).ConclusionHigher levels of DII may be associated with occurrence of early kidney damage. For individuals with hypertension, avoiding excessive consumption of pro-inflammatory foods may reduce the risk of renal injury.

Abstract Background Chronic kidney disease (CKD) and overweight/obesity are significant global public health issues. Appropriate free-time physical activity (PA) is essential for overweight/obese patients with chronic kidney disease, but specific guidelines are lacking. The present study was conducted to determine the association between PA and all-cause mortality in these patients. Methods Data from 3,434 overweight/obese adults with CKD from the 1999–2016 National Health and Nutrition Examination Surveys were analyzed. Associations between clinical/laboratory findings and PA intensity (moderate and vigorous) were investigated. The all-cause mortality of patients in different PA categories were compared by Kaplan–Meier analysis. Factors associated with all-cause mortality were determined using a Cox proportional hazards model. A restricted cubic spline was employed to obtain a more flexible and detailed representation of the relationship between PA intensity and all-cause mortality, with better predictive capability. Results The Kaplan–Meier analysis revealed that greater all-cause mortality was associated with < 10 min/week moderate/vigorous PA (log-rank p < 0.001). A greater survival probability was associated with ≥ 150 min/week vigorous PA or 10–149 min/week moderate PA (log-rank p < 0.001). Age, gender, vigorous PA, smoking status, alcohol consumption, diabetes status, eGFR, serum albumin level, uric acid level, and blood urea nitrogen level were identified as factors associated independently with mortality in the Cox proportional hazards analysis. The restricted cubic splines revealed that these relationships were non-linear (all p < 0.05). Kaplan–Meier analysis of data from patients who engaged in 10–450 min/week moderate/vigorous PA revealed significant differences between the 0–74-min/week and other vigorous PA groups (all log-rank p < 0.001). Conclusions Extended durations of vigorous PA are associated with reduced all-cause mortality in overweight/obese patients with CKD. Clinicians should recommend vigorous free-time PA to these patients, and public health interventions should target this goal to maximize patient health.

BackgroundImmunoglobulin A nephropathy (IgAN) is the most prevalent form of chronic kidney disease (CKD), marked by diverse pathological patterns and variable prognostic outcomes. Nutritional indexes are crucial for disease assessment and prognosis prediction. This study investigates associations between nutritional indexes and renal function in patients with IgAN.MethodsA cohort of 736 adults diagnosed with IgAN, who underwent renal biopsy at the First Hospital of Jilin University between January 2010 and October 2022, was examined. Clinical and laboratory data were reviewed, and four nutritional indexes were calculated: controlling nutritional status (CONUT) score, geriatric nutritional risk index (GNRI), body mass index (BMI), and prognostic nutritional index (PNI). Cox-proportional hazard analysis evaluated factors associated with end-stage renal disease (ESRD).ResultsPatients with ESRD showed significantly lower GNRI (91.84 vs. 98.94, p < 0.001) and median PNI (41.90 vs. 46.30, p < 0.001), with higher median CONUT score (2.00 vs. 1.00, p = 0.001) compared to those without ESRD. PNI, GNRI, and CONUT scores correlated significantly with C2 in MEST-C classification. Kaplan–Meier analysis indicated increased ESRD probability in individuals with specific thresholds of PNI, GNRI, or CONUT scores. Additionally, GNRI emerged as an independent predictor of ESRD (hazard ratio: 0.963, 95% CI: 0.940–0.979, p < 0.001), along with platelet count, serum creatinine, eGFR (CKD-EPI), and triglyceride levels.ConclusionGNRI, PNI, and CONUT scores hold potential in reflecting IgAN severity and predicting ESRD risk. GNRI especially may serve as a valuable tool for identifying high-risk individuals for ESRD in IgAN.

Silica nanoparticles (SiNPs) are nanomaterials with widespread applications in drug delivery and disease diagnosis. Despite their utility, SiNPs can cause chronic kidney disease, hindering their clinical translation. The molecular mechanisms underlying SiNP-induced renal toxicity are complex and require further investigation. To address this challenge, we employed bioinformatics tools to predict the potential mechanisms underlying renal damage caused by SiNPs. We identified 1627 upregulated differentially expressed genes (DEGs) and 1334 downregulated DEGs. Functional enrichment analysis and protein-protein interaction network revealed that SiNP-induced renal damage is associated with apoptosis. Subsequently, we verified that SiNPs induced apoptosis in an in vitro model of NRK-52E cells via the unfolded protein response (UPR) in a dose-dependent manner. Furthermore, in an in vivo rat model, high-dose SiNP administration via tracheal drip caused hyalinization of the renal tubules, renal interstitial lymphocytic infiltration, and collagen fiber accumulation. Concurrently, we observed an increase in UPR-related protein levels at the onset of renal damage. Thus, our study confirmed that SiNPs induce apoptosis and renal damage through the UPR, adding to the theoretical understanding of SiNP-related kidney damage and offering a potential target for preventing and treating kidney injuries in SiNP clinical applications.

Abstract Silica nanoparticles (SiNPs) have multiple applications, particularly in the field of biomedical science. However, SiNPs can cause a multitude of diseases, including chronic kidney disease (CKD). The molecular mechanism of renal toxicity caused by SiNPs is complex and remains to be clarified. Therefore, we examined the role and mechanism of apoptosis via the unfolded protein response (UPR) induced by SiNPs. We utilized an in vitro model of NRK-52E cells and an in vivo rat model with SiNPs administered via tracheal drip. After the NRK-52E cells were exposed to SiNPs, cell viability decreased; the mitochondrial membrane potential, calcium content, reactive oxygen species, and apoptosis rate increased; and light microscopy revealed cell damage. Meanwhile, apoptosis, the UPR, and oxidative stress-related proteins were all increased in NRK-52E cells. Moreover, an increase in the concentration of SiNPs was positively correlated with renal damage, as detected by light microscopy and transmission electron microscopy. As the SiNP concentration increased, apoptosis, the UPR, and oxidative stress-related proteins increased and the activity of antioxidant enzymes decreased in rat kidney. We conclude that the UPR plays a key role in apoptosis induced by SiNPs in the kidney.

Hypothyroidism is a prevalent endocrine illness with a variety of clinical symptoms, but among which elevated serum creatinine is uncommon. Hypothyroidism is also common in acquired immunodeficiency syndrome (AIDS) patients, especially those receiving highly active antiretroviral treatment (HAART). Here we present a case of a young AIDS patient with hypothyroidism, increased serum creatinine, and obesity. Despite the lack of a kidney biopsy, following levothyroxine (LT4) therapy, his serum creatinine recovered to normal levels, and weight loss, edema, weakness, rough skin and other clinical symptoms obtained notable improvement. This highlights the need of clinicians paying attention to whether thyroid function is aberrant in human immunodeficiency virus (HIV) patients with increased creatinine, edema and significant weight gain since prompt thyroid hormone therapy can restore the alterations in renal function and avoid invasive renal biopsy.

慢性肾脏病( CKD )在普通人群的发病率为10％ ～13％ 〔1,2〕. 随着年龄的增长, CKD 的危险因素如糖尿病、高血压等发生率增加,导致老年CKD发病率明显增加. 美国NHANES 2011 ～2012 年调查数据显示,65～79岁CKD发病率为31. 5％,80岁及以上CKD发生率高达65％ 〔3〕.

医患沟通( doctor-patient communication)是临床医疗活动的重要环节,也是参加规范化培训的住院医师所必须掌握的技能. 医患沟通是指医患双方在医疗活动中,针对疾病的诊疗、健康宣教、跟踪随访等方面进行的多途径交流,其中也包含了医患双方在情感、思想、治疗期望等方面的诉求. 医患沟通旨在建立信任、合作的医患关系,进而获得满意的诊疗效果[1-2]. 建立良好的医患沟通,不仅可以构建和谐的医患关系、减少医疗隐患及纠纷、提高医疗服务质量,同时也是培养合格医学人才的必经之路. 文章总结了住培医师医患沟通能力的培养目标,分析了影响住培医师医患沟通能力的不利现状,并提出了提高住培医师医患沟通能力的具体措施,以便为培养具有医患沟通能力和医学人文素养的住培医师提供参考.

住院医师规范化培训是医学生毕业后正式进入临床工作前的重要临床教育阶段,在此阶段切实有效地培养临床实践技能至关重要.文章分析了完全以临床患者为实践对象的种种弊端,引入了角色扮演以及情景模拟教学的概念,总结了角色扮演结合情景模拟教学法在肾内科住院医师规范化培训临床带教中的诸多优势,并以高钾血症为例提出了角色扮演结合情景模拟教学法的实施方案,具体包括:编写情景模拟案例、实施过程、小组讨论以及归纳总结,指出角色扮演结合情景模拟教学法可以取得较好的住院医师规范化培训教学效果,具有实际应用价值.

目的:探讨同时应用利福平和降压药物患者血压异常升高病例的诊疗过程,分析利福平与降压药物的相互作用,提高临床医生对该类患者用药的认识.方法:收集1例同时服用利福平和降压药物患者的临床资料,分析患者血压变化与药物的关系,结合相关文献,观察利福平作用后二氢吡啶类钙离子拮抗剂血药浓度的变化.结果:患者,男性,58岁,因咳嗽、咳痰1个月入院.入院前患者被明确诊断为肺结核、高血压,同时服用利福平、异烟肼、乙胺丁醇、吡嗪酰胺和非洛地平,入院后继续原治疗方案并予以监测血压.抗结核病治疗第9天患者出现头晕和胸闷,血压剧烈波动,予以停用利福平、调整降压药物等对症支持治疗.患者血压波动初期,联合血管紧张素转换酶抑制剂及加强二氢吡啶类钙拮抗剂用量的治疗并未使血压升高得到控制,停用利福平后36 h血压开始明显下降,于抗结核治疗第18天恢复原降压方案治疗,患者血压保持稳定.结论:利福平有时可明显降低降压药物(如二氢吡啶类钙拮抗剂)的降压效果,应引起临床医生的重视.

患者,女,67岁,因间断腹泻4个月,四肢皮肤色素沉着,指(趾)甲发黄、变形2 个月,加重1 个月于2016年8月15 日就诊于我院胃肠内科.患者4个月前无明显诱因出现腹泻,每日3~4次,黄色水样便. 2个月前出现脱发、四肢皮肤色素沉着,指(趾)甲变厚、发黄、卷曲,指趾末端增粗. 1月前腹泻加重,每日7 ~8 次,伴血便,全腹隐痛,脐周明显,伴里急后重感,便后腹痛略缓解,于外院做肠镜示全结肠黏膜多发鹅卵石样突起,行抗感染、止泻、对症治疗,病情略缓解. 病程中,伴乏力、味觉减退,体重减轻约 5 kg. 既往吸烟史 20年. 家族史无特殊. 查体: 体温36.7℃,心率84 次/min,呼吸18 次/min,血压101/74 mmHg,颜面轻度浮肿,灰暗,散在棕色斑点,深浅大小不一,毛发枯燥,易脱落,带毛囊,舌乳头萎缩,舌面光滑如镜,四肢色素沉着,指(趾)甲增厚,粗糙、色黄、卷曲,指(趾)端杵状增生(图 1). 辅助检查:钾2.73 mmol/L,血清白蛋白26.5 g/L;促甲状腺激素26.08 uIU/mL,游离 T33.28 pmol/L,游离 T410.63 pmol/L;超敏C反应蛋白8.34 mg/L;便潜血阳性;先后送检粪便培养 3次,第 1 次为大量白假丝酵母菌,其余2 次阴性;抗小肠杯状细胞抗体IgG、IgA 1:32 阳性. 2016 年7 月11日行胃镜检查:胃窦各壁广泛分布颗粒状黏膜突起;病理示黏膜慢性炎症;幽门螺旋杆菌阴性.