ObjectiveA new Tripterygium wilfordii preparation called Kunxian capsule (KX) has been approved in China. However, it is still unknown whether KX is safe and effective for idiopathic membranous nephropathy (IMN) and its therapeutic mechanism of action is unclear.MethodsWe conducted a retrospective study of 39 patients with IMN who received KX to investigate its efficacy and side effects of KX in treating IMN. We also used network pharmacology and molecular docking methods to explore the potential mechanism of action of KX in IMN.ResultsIn patients with IMN receiving KX treatment, 24 h urine protein was markedly decreased, whereas serum albumin levels increased. The overall clinical response rate was 79.49% after 6 months of treatment, and there were no significant adverse events. Quercetin, luteolin and kaempferol were the main bioactive ingredients of KX in treating IMN. AKT1, IL6, and TNF were core targets. The main potential mechanism of KX in treating IMN were pathways involved in cancer, the AGE-RAGE signaling pathway in diabetic complications, lipid and atherosclerosis. Molecular docking results showed that the binding force between the active ingredient and core target was relatively stable.ConclusionKX is a safe and effective treatment option for IMN and can effectively improve serum albumin and 24 h urine protein levels in patients with IMN. This study preliminarily reveals the possible mechanism of KX in the treatment of IMN and provides a theoretical basis for future clinical research.

IgA nephropathy (IgAN) is the most common cause of primary glomerulonephritis, with complex pathogenic mechanisms involving abnormal B-cell activation. Women with IgAN are at a higher risk of adverse pregnancy outcomes such as preeclampsia and miscarriage, especially those with uncontrolled massive proteinuria and advanced chronic kidney disease. Therefore, IgAN disease control before and during pregnancy is essential. Telitacicept inhibits both B-lymphocyte stimulating factor and a proliferation-inducing ligand. It also inhibits both B cells and plasma cells and the production of galactose-deficient IgA1 (Gd-IgA1) and its autoantibodies, thus exerting an immunosuppressive effect. We report the case of a woman with IgAN who had a successful pregnancy with significant improvement and long-term remission after treatment with telitacicept. Based on clinical manifestations, laboratory analysis and pathological results, the patient was diagnosed as IgAN.We mainly used telitacicept during her treatment,and conducted long-term follow-up. A 32-year-old female was found to have 3+ urinary protein levels in 2016 but did not receive any specific treatment. A follow-up examination in 2019 revealed a 3+ urinary protein level, 3+ urinary blood level, and serum creatinine level of 90 µmol/L. The outpatient physician prescribed the maximum tolerated dose of the renin-angiotensin-aldosterone system (RAAS) inhibitor valsartan (150 mg orally once daily). In September 2021, the patient was hospitalized due to proteinuria and hematuria, and a renal biopsy confirmed the diagnosis of IgAN (Lee classification, grade 3; Oxford classification, M1E1S1T0). The patient was prescribed oral prednisone acetate (50 mg/day). In October 2021, the patient's creatinine, urinary protein, urinary erythrocytes, and leukocytes in the blood increased significantly, with a possible urinary tract infection, likely related to long-term administration of steroid therapy. The patient expressed a desire to avoid the side effects of high-dose steroids use, as well as a strong desire to conceive and, therefore, hoped that the disease could be controlled as quickly as possible. After 1 week of admission for infection control, we treated her with steroid therapy combined with telitacicept. After 1 week of telitacicept treatment, the patient's proteinuria, hematuria, and creatinine level decreased significantly. Since then, her 24-h proteinuria had remained stable at less than 0.5 g. We adjusted the dosage of steroids and telitacicept according to the patient's condition. Following the successful reduction of the dose of prednisone acetate to 10 mg, the dosage was slowly tapered to 0 mg. The treatment course is presented in Fig. 1. She received her last dose of telitacicept on June 17, 2022; at the same time, the prednisone acetate was also discontinued. However, the patient became pregnant 3 months after stopping the medication. After a comprehensive evaluation by the obstetrician and nephrologist and after explaining the potential risks to the patient, the patient requested to continue the pregnancy. The patient's 24 h proteinuria remained consistently below 0.5 g during pregnancy, her blood creatinine was stable at 70–95 µmol/L, her urine erythrocytes were stable at 5–18/µL, and her blood pressure was within the normal range, weight gain during pregnancy 15 kg. On June 5, 2023 (39 week and 3 days of pregnancy), she delivered a boy, weighing 2750 g and measuring 41 cm, with an Apgar score of 9 at 1 min and 10 at 5 min. Considering the patient's need for breastfeeding, we administered hydroxychloroquine 200 mg/dose twice daily oral maintenance therapy. Thereafter, the patient's condition stabilized. From the start of telitacicept treatment until the last follow-up at our hospital on on September 23, 2024, she had no recurrence of the disease, and her condition was significantly controlled (Table 1). This report describes the efficacy of telitacicept in patients with IgAN and explores its value in women of childbearing age, suggesting effective and safe treatment options for women who wish to conceive.

Objective: To elucidate the potential causality of leukocyte telomere length (LTL) with immune-mediated inflammatory diseases (IMIDs), we conducted a Mendelian randomization (MR) study.Methods: The genetically predicted causation between LTL and IMIDs was evaluated using a two-sample MR method. We analyzed 16 major IMIDs, which included systemic lupus erythematosus (SLE), inflammatory bowel disease (IBD), ulcerative colitis (UC), Crohn’s disease (CD), ankylosing spondylitis (AS), sicca syndrome (SS), rheumatoid arthritis (RA), type 1 diabetes (T1D), primary sclerosing cholangitis (PSC), idiopathic pulmonary fibrosis (IPF), atopic dermatitis (AD), sarcoidosis, hypothyroidism, hyperthyroidism, psoriasis, and childhood asthma. The random-effects inverse-variance weighted (IVW) method was performed as the main analytical approach in MR. Various sensitivity analyses, including MR-Egger, MR robust adjusted profile score (MR-RAPS), weighted median, MR pleiotropy residual sum and outlier (MR-PRESSO) methods, weighted mode, radial plot, and radial regression, were used to guarantee the robustness of the results and detect horizontal pleiotropy. Cochran’s Q value was calculated to check for heterogeneity, and the MR Steiger approach was used to test the causal direction.Results: The MR results indicated significant inverse associations of LTL with risks of psoriasis (OR: 0.77, 95% CI: 0.66–0.89, and p = 3.66 × 10−4), SS (OR: 0.75, CI: 0.58–0.98, and p = 0.03), RA (OR: 0.77, 95% CI: 0.68–0.88, and p = 9.85 × 10−5), hypothyroidism (OR: 0.84, 95% CI: 0.78–0.91, and p = 7,08 × 10−6), hyperthyroidism (OR: 0.60, 95% CI: 0.44–0.83, and p = 1.90 × 10−3), sarcoidosis (OR: 0.67, 95% CI: 0.54–0.83, and p = 2.60 × 10−4), and IPF (OR: 0.41, 95% CI: 0.29–0.58, and p = 4.11 × 10−7) in the FinnGen study. We observed that longer LTL was associated with an increased risk of AS susceptibility (OR: 1.51, 95% CI: 1.18–1.94, and p = 9.66 × 10−4). The results of the IVW method showed no causal relationship between TL and SLE (OR: 0.92, 95% CI: 0.62–1.38, and p = 0.69) in the FinnGen study; however, a significantly positive correlation was shown between LTL and SLE in another larger GWAS (OR: 1.87, 95% CI: 1.37–2.54, and p = 8.01 × 10−5).Conclusion: Our findings reveal that abnormal LTL has the potential to increase the risk of IMIDs. Therefore, it could be treated as a predictor and may provide new potential treatment targets for IMIDs. However, the change of LTL may not be the direct cause of IMIDs. Further studies should aim at the pathogenic mechanism or potential protective effects of LTL in IMIDs.

The present study aimed to detect the levels of microRNA (miR)-33a-5p in the renal tissue, serum and urine of patients with primary IgA nephropathy (IgAN), thereby preliminarily exploring the association between the levels of miR-33a-5p and the condition of primary IgAN to provide evidence for the expression of miR-33a-5p in the serum and urine of IgAN patients as a clinical marker. Reverse-transcription quantitative PCR was performed to evaluate the level of miR-33a-5p in IgAN patients according to severity and pathological classification. The results suggested that the levels of miR-33a-5p in the serum, urine and kidney tissues of patients with IgAN were lower than those of the control tissues obtained from cancer patients (0.28±0.25 vs. 1.00±0.45, P<0.05; 0.34±0.28 vs. 1.00±0.53, P<0.05; 0.47±0.27 vs. 1.00±0.38, P<0.05, respectively). Receiver operating characteristic curve analysis suggested that the serum and urine levels of miR-33a-5p may be used as a marker to differentiate renal injury in IgAN patients from healthy individuals. At the same time, according to the estimated glomerular filtration rate (eGFR) and Lee classification of nephropathy, it was determined that with the progression of renal failure and the increase of the pathological grade of kidney tissue, the relative level of miR-33a-5p in kidney tissue also decreased (eGFR <50 ml/min vs. eGFR ≥50 ml/min/1.73 m2 group: 0.38±0.27 vs. 1.00±0.34, P<0.001; Lee grade ≤3 group vs. Lee grade >3: 1.00±0.48 vs. 0.38±0.45, P<0.05). This result suggested that the levels of miR-33a-5p in serum, urine and kidney tissues decreased with the severity of renal injury and the progression of renal failure in patients with IgAN. Hence, miR-33a-5p detected in the serum and urine may be used as a non-invasive biomarker to reflect the progression of renal injury and renal failure in patients with IgAN.

Chronic kidney disease (CKD) has a worldwide prevalence of 8%-16%. Renal interstitial fibrosis is the main route of CKD progression, and eventually inevitably develops into end-stage renal disease (ESRD), causing a huge socioeconomic burden. In recent years, mesenchymal stem cells (MSCs) have shown great potential in repairing injury by their multi-directional differentiation and self-renewal ability. Recent studies have found that MSCs can regulate renal interstitial fibrosis-related signaling pathways through the immune response and paracrine effects, inhibit tubular epithelial-mesenchymal transition (EMT), and thereby delay renal interstitial fibrosis. This article reviewed the mechanism, related researches, and existing challenges of MSCs in delaying renal interstitial fibrosis.

Collagen type III is commonly detected in the renal interstitium and vasculature; however, it is absent in healthy glomeruli. Deposition of collagen type III in the glomerular mesangium and capillary basement membranes may arise in two rare diseases, namely collagen type III glomerulopathy (CG) and nail patella syndrome. CG is a rare glomerular disease with no specific treatment, although supportive measures for control of hypertension and edema may help to relieve symptoms. With progression to end-stage renal disease, patients with CG may come to require dialysis and/or renal transplantation. The present study reported on a 59-year-old male who was diagnosed with CG nephrotic syndrome by immunohistochemical and electron microscopic examination of biopsy material. To the best of our knowledge, this is the first case reported in northeastern China. The angiotensin II blocker telmisartan was successfully used to alleviate renal symptoms and a literature review was performed. The present case supports the use of telmisartan as a first choice of treatment for CG.

Hemodialysis (HD) is the most important treatment for patients with end‐stage renal disease (ESRD). Thrombocytopenia is a potential treatment complication related to dialysis. Under normal circumstances, the platelet count would slightly decrease within the first hour of HD, but get restored towards the end of procedure. In most patients, the platelet count can be maintained within the normal range, and the occurrence of thrombocytopenia is relatively rare in clinical practice. Therefore, the possibility of thrombocytopenia in HD patients is often ignored. Moreover, thrombocytopenia might be misdiagnosed and mistreated. At present, almost all articles on the subject, apart from some case reports, focus on pseudothrombocytopenia and heparin‐induced thrombocytopenia. In this review, we summarized various underlying causes, mechanisms, and diagnostic approaches to thrombocytopenia in HD patients. The review aims to provide a guide for clinicians interested in the causes and adequate treatment of thrombocytopenia.

患者,女,48岁,因“发现尿常规异常1年,血肌酐升高6天”于2017年11月6日入院.患者1年前体检时发现尿潜血(+++),口服“血尿胶囊”(具体剂量不详)后好转.3个月前再次体检,尿常规检查结果示潜血(+++)、尿蛋白(++),血肌酐正常,未予系统诊治.6天前于外院尿常规检查结果显示潜血(++)、尿蛋白(+)、葡萄糖(+++),血肌酐84.4 μmol/L(括号内为正常值,以下相同,41.0～ 73.0 μmol/L),尿酸60 μmol/L(89～375 μmol/L),为求进一步诊治遂来我院.

Transmembrane protein 158 (TMEM158) plays pivotal roles in many cancers, including colorectal cancer (CRC). It has been reported that it is a recently identified upregulated gene during Ras-induced senescence. However, the clinical significance and biological functions of TMEM158 in CRC remain largely unknown. In this study, we found that TMEM158 was highly expressed in CRC tissues and cell lines compared with the corresponding noncancerous samples and normal colon epithelial cells. In vitro studies showed that TMEM158 silencing inhibited proliferation, and migration and increased apoptosis of CRC cells, whereas overexpression of TMEM158 increased proliferation, migration, and apoptosis escape of CRC cells. Mechanically, the levels of drug resistance-associated molecules, including multidrug resistance 1 and multidrug resistance protein 1, as well as the expression of antiapoptotic Bcl-2 were significantly upregulated. In addition, TMEM158 knockdown significantly inhibited tumor growth in vivo. Collectively, these results demonstrated that TMEM158 is a significant regulator of tumorigenesis and drug resistance in CRC and provided evidence that TMEM158 may be a promising target for CRC therapy.

BACKGROUND:The current study aims to observe the correlation between the expression of miR-152-5p in urine samples and the condition of IgA nephropathy (IgAN).METHODS:From January 2017 to October 2017, 40 patients with IgAN, 10 patients with mild glomerular lesions, 10 patients with membranous proliferative glomerulonephritis type I, 10 patients with focal segmental glomeruloscle-rosis, 10 patients with Henoch-Schonlein purpura nephritis, and 10 patients with lupus nephritis. Meanwhile, 25 healthy controls were also included in the physical examination center of our hospital. The expression level of miR-152-5p was detected by RT-qPCR. The correlation between the expression level of miR-152-5p and patholog-ical Haas grading and urinary protein was analyzed.RESULTS:The expression level of miR-152-5p in IgA nephropathy patients was higher than that in other types of glomerulonephritis and healthy control group (p < 0.0001). Meanwhile, the level of miR-152-5p in IgAN patients with high score (p < 0.01) was significantly increased. Furthermore, the level of miR-152-5p was positively corre-lated with the level of urinary protein and the degree of renal pathological damage (r2 = 0.89, p < 0.01).CONCLUSIONS:The expression of urinary miR-152-5p is positively correlated with IgA nephropathy, which provides a new way for early diagnosis and treatment of IgA nephropathy with elevated proteinuria.

In recent years, the Wnt/β-catenin signaling has gained tremendous attention due to its ability to modulate a number of diseases including diabetic nephropathy. Studies have shown that there is decrease in the secretion of Wnt proteins including Wnt4, 5a and Wnt 6 during high glucose concentration or diabetic conditions, which leads to decreased translocation of β-catenin to nucleus. The down-regulation of Wnt/β-catenin signaling leads to detrimental effects on kidney including increased apoptosis of mesangial cells and increased deposition of fibrous tissue in mesangium. The pharmacological modulators such as spironolactone, NO donor and antioxidant are shown to produce beneficial effects in diabetic nephropathy by up regulating the expression of Wnt proteins and activation of diabetes-induced suppressed Wnt/β-catenin signaling. On the other hand, it is documented that diabetes leads to overactivation of Wnt1/β-catenin signaling, which promotes podocyte injury, induce epithelial-mesenchymal transition of podocytes along with renal injury and fibrosis. Accordingly, different interventions aimed to suppress overactivated Wnt/β-catenin signaling are reported to improve the condition and symptoms associated with diabetic nephropathy. The present review discusses the dual role of Wnt/beta-catenin signaling in the pathogenesis of diabetic nephropathy.

Objective To evaluate the clinical efficacy and safety of the following different treatment regimens for idiopathic membranous nephropathy（IMN）: modified Ponticelli regimen(MPR, alternating therapy of hormone（Prednisone,Pre） combined with Cyclophosphamide（CTX）, prednisone combined with CTX（Pre/CTX） and prednisone combined with Tacrolimus（Pre/TAC）. Methods A total of 67 patients diagnosed with IMN by kidney biopsy from the 2nd Hospital of Jilin University were analyzed on their clinical information about urine protein and albumin. Based on the treatment regimens, they were divided into MPR group, Pre/CTX group and Pre/TAC group. All the patients were treated for 6 months. We observed clinical efficacy in the three groups for 3-month and 6-month treatment, and monitored adverse reactions during the treatment course. Results No significant difference was observed at baseline before treatment. After 3-month treatments, in the MPR group, 8（34.7%） of 23 patients reached partly remission and the effectiveness rate is 34.7%; in the Pre/CTX group, 1（4.2%） of 24 patients died, 1（4.2%） reached complete remission, 8（33.3%） reached partly remission and the effectiveness rate is 37.5%; and in the Pre/TAC group, 8（40.0%） of 20 Pre/TAC group patients reached partly remission and the effective rate is 40.0%. The above results in the three groups have no statistical difference. After 6-months treatments, in the MPR group, 1（4.3%） of 23 patients died, 1（4.3%） of the rest 22 patients reached complete remission, 12（52.2%） reached partly remission and the effectiveness rate is 56.5%; in the Pre/CTX group, 2（8.7%） of the rest 23 patients reached complete remission, 17（73.9%） reached partly remission and the effective rate is 82.6%; and in the Pre/TAC group, 1 of 20 patients（5.0%） reached complete remission, 12（60.0%） reached partly remission and the effective rate is 65.0%. The results in the 3 groups have no statistical difference. MPR had less adverse reactions during the treatments. ConclusionsMPR, Pre/CTX and Pre/TAC regimens have comparable effectiveness for IMN; the MPR regimen is characterized by short treatment course and less prednisone accumulation dose, and so may have a high level of safety.

慢性肾脏病( CKD)的定义包扩两层含义,一是指肾脏损伤(肾脏结构或功能异常)≥3个月,伴或不伴有肾小球滤过率(GFR)下降,二是指GFR≤60 ml·min-1·1.73 m-2≥3个月,有或无肾脏损伤证据。根据GFR水平,慢性肾脏病可分为五期,CKD5期即为终末期肾病(ESRD),需肾脏替代治疗。 CKD合并心房颤动在临床上常见,其发生率约19%~24%[1]。Wang等[2]研究了1168例慢性肾脏病( CKD)住院患者,分组比较房颤的患病率,得出估算肾小球滤过率( eGFR)、透析与房颤显著相关的结论。 CKD患者合并房颤的患者发生血栓栓塞的风险比单纯房颤患者增加了近50%,并且血栓栓塞风险与肾功能下降程度相关[3]。抗凝治疗能有效降低房颤患者血栓栓塞的发生率,进而降低患者的死亡率、改善房颤患者长期预后,推荐CKD合并AF的患者抗凝治疗；而CKD患者抗凝治疗出血风险较单纯房颤大,故CKD合并房颤抗凝治疗有重要的临床意义。本文综述CKD合并心房颤动抗凝治疗的研究现状。心房颤动抗凝治疗包括药物治疗和非药物治疗,药物治疗包括传统的维生素K拮抗剂(华法林)及新型抗凝剂(达比加群、利伐沙班、阿哌沙班)。非药物治疗指左心耳封堵术。

Diabetic nephropathy (DN) is one of the most common diabetic microvascular complications and is defined as a rise in urine albumin excretion (UAE) rate and progressive renal function loss. Now albuminuria is considered the gold standard of onset or progression of DN. However albuminuria has certain limitations, clinical practice suggested detectable albuminuria is later than the onset of DN and subsequent intervention could not block the progression of DN effectively, which could lead to renal function deterioration influencing morbidity and mortality. Thus, the request for more reliable highly sensitive and specific biomarkers is needed for early predicting the onset and progression of DN, which is important to slow down or prevent the renal function decline in diabetic patients. Tremendous studies have implicated lots of biomarkers associated with DN could be applied to predict the onset or monitor the progression of DN. In this review, we summarize and screen a lot of already known biomarkers, the newly reported biomarkers in urine and serum,such as serum sKloth, Serum angiopoietin-like protein 2 (Angptl2), and urinary vitamin D-binding protein (VDBP), predicting development and progression of DN, which could be potential useful tools in the management of DN.

本研究选择2005年1月-2012年12月在我院住院并进行肾活检的486例继发性肾小球疾病患者,探讨继发性肾小球疾病性别、病理类型分布特征、病理类型与临床表现的关系,旨在为临床肾脏疾病的诊断、治疗及预后判断提供有价值的资料。1资料与方法1.1一般资料选择2005年1月-2012年12月于我院肾病内科住院行肾穿刺活检486例继发性肾小球疾病患者,患者的临床及病理资料均完整、属实,

<正>酒精性肝硬化导致的意识障碍与肝性脑病的临床表现很相似,表现为意识障碍,性格行为变化,冷漠或欣快,哭、大笑、错乱穿衣、计算力、理解力、定向力、记忆力减退等行为。但是在B超的影像中酒精性肝硬化导致的意识障碍与肝性脑病却很容易鉴别。2012年5月10日,我院门诊将酒精性肝硬化误诊为肝性脑病1例,收入院治疗。患者在入院前没做B超,而

<正>老年病毒性肝炎是严重危害患者健康的传染病,并且有逐年增加的趋势。到目前为止,世界各国还没有特效的治疗方法。有些患者认为,一旦感染上肝炎病毒,就会发展为肝炎——进一步发展为肝硬化,最终导致肝癌,成为绝症。尤其是老年病毒性肝炎,由于老年人生理功能相应减退,肝细胞再生能力差,肝脏的解毒能力及代谢功能降低,免疫功能下降。心、肾等重要脏器可能存在慢性疾病或有潜在病变等,使得病

<正>发生输液反应的原因有很多种。2011年5月23日,我院1名患者在静点完长春海悦药业有限公司生产的促肝细胞生长素注射液后5～10min,突然出现头晕、恶心、呕吐、大汗淋漓、呼吸困难、四肢厥冷等现象,随即出现意识丧失、口唇及双手明显紫绀。经调查是静点促肝细胞生长素注射液过敏性反

患者女,37岁.明确诊断系统性红斑狼疮(SLE)1年,胸闷、气短、不能平卧7d入院.患者1年前因阴道不规则流血,色深红,有血块就诊于我院,详细询问病史,患者有口腔溃疡及脱发表现,当时辅助检查:血常规示:血红蛋白38 g/L,血小板70.0×109/L;尿常规示:尿蛋白(+++);抗核抗体1:320,明确诊断为"SLE,狼疮肾炎,慢性肾功能不全-肾衰竭期",开始应用糖皮质激素治疗(甲泼尼龙40 mg静脉滴注),并于我院行动静脉内瘘成形术,内瘘成熟后开始规律血液透析,每周3次,病情平稳,其后糖皮质激素逐渐减量至泼尼松7.5 mg口服;高血压病史1年,目前血压控制尚可.