FK506治疗肾炎与生化指标的三维图像分析

观察新型免疫抑制剂FK506(普乐可复)对狼疮性肾炎(IV+V)的疗效与体内血糖、白蛋白、血红蛋白、红细胞、年龄、血钾、血钠指标的关系。针对在我院临床诊断为肾病综合征、病理诊断为狼疮性肾炎(IV+V)的患者,应用普乐可复(口服剂量0.15~0.3mg/kg/d 2/日)进行治疗。对其血药浓度进行检测,根据血药浓度调整剂量。治疗后患者24小时尿蛋白转阴。新型免疫抑制剂普乐可复有望成为狼疮性肾炎治疗的安全、有效的方法之一。     

多靶点对狼疮性肾炎的治疗研究

目的针对多靶点治疗狼疮性肾炎的临床疗效展开分析研究。方法选取我院2005年至2009年收治的确诊为狼疮性肾炎患者50例,整理临床资料,依据肾炎治疗方式分为普通观察组(25例)和多靶点组(25例)。普通观察组在整个治疗过程中给予环磷酰胺加入0.9%氯化钠注射液中静滴或静注。而多靶点对照组采用霉酚酸酯(MMF)联合中小剂量泼尼松治疗,并给予环磷酰胺(CTX)冲击治疗,三联法多靶点治疗狼疮性肾炎。结果多靶点对照组治疗效果优于普通观察组,多靶点对照组总治愈率为91.3%,普通观察组治愈率为34.78%。结论在整个治疗过程中运用霉酚酸酯(MMF)联合中小剂量泼尼松治疗,并给予环磷酰胺(CTX)多靶点治疗,为狼疮性肾炎患者减轻了疾病上的疼痛,治愈率高,安全性大。所以,多靶点治疗在临床上是有效、可观的治疗方法,是值得临床推广的一种治疗方法。     

他克莫司治疗狼疮性肾炎(Ⅳ+Ⅴ型)1例的病理图像与用药分析

观察新型免疫抑制剂他克莫司对狼疮性肾炎(Ⅳ+Ⅴ)的疗效。1例在我院肾科临床诊断为肾病综合症、病理诊断为狼疮性肾炎(Ⅳ+Ⅴ)的女性患者,应用他克莫司(口服剂量为0.15～0.3mg/kg/d 2/日)进行治疗。对其血药浓度进行检测,根据血药浓度调整剂量。治疗2周后患者24小时尿蛋白转阴。新型免疫抑制剂他克莫司有望成为狼疮性肾炎治疗的安全、有效的方法之一。     

老、中、青肾移植患者口服普乐可复后总胆红素、尿酸、服药天数的三维图像分析

研究分析老、中、青年肾移植患者服用普乐可复天数、总胆红素、尿酸的三维图像,使临床指标形象化显现,为预测疾病提供信息。将60岁以上老年患者、40~59岁中年患者与小于40岁青年患者分三组,采用MATLAB7.0做三维图像,分析图像特征并且对老年、中年、青年组图像进行比较。三维图像显示出各项指标间存在内在关系与个体差异。体内指标与服药天数相关,体内指标对临床预防疾病具有重要意义。     

黄芪联合百令胶囊治疗紫癜性肾炎疗效观察

目的探讨黄芪注射液联合百令胶囊治疗过敏性紫癜性肾炎的疗效。方法将100例过敏性紫癜性肾炎随机分为治疗组50例、对照组50例,对照组及治疗组均给予氯雷他啶、芦丁、维生素C、葡萄糖酸钙抗过敏治疗,治疗组加用黄芪注射液20～30mL/次、5%葡萄糖注射液稀释静滴、1次/d,百令胶囊0.6～1.0(3～5粒),每日3次口服。结果治疗组过敏性紫癜性肾炎患者症状,尿潜血,尿蛋白定性改善优于对照组,2组疗效具有显著性差异(P<0.05)。结论黄芪注射液联合百令胶囊治疗过敏性紫癜性肾炎疗效显著。     

稳心复脉汤联合西药心律平治疗快速心律失常疗效观察

目的观察稳心复脉汤联合西药心律平治疗快速心律失常的临床疗效。方法将76例快速心律失常患者随机分为治疗组51例口服稳心复脉汤加心律平胺碘酮,对照组25例单独服用稳心复脉汤。疗程均为4周。结果治疗组的疗效均明显好于对照组,其余各证型之间无差别。对照组治疗各证型的疗效无明显差异。结论对比较严重的心律失常及初诊心律失常选用稳心复脉汤联合心律平胺碘酮常规治疗疗效更好;对病程长需长期服药的心律失常患者选用稳心复脉汤效果好副反应少     

莫匹罗欣软膏联合阿达帕林凝胶治疗寻常型痤疮临床观察

目的观察莫匹罗欣软膏联合阿达帕林凝胶治疗寻常型痤疮的临床疗效和安全性。方法寻常型痤疮60例,随机分为两组。治疗组30例,外用莫匹罗欣软膏,每日1次,外用0.1%阿达帕林凝胶,每晚1次,连用8周;对照组30例,外用0.1%阿达帕林凝胶,每晚1次,连用8周。停药后观察其疗效。结果治疗组痊愈11例,显效13例,总有效率为80%;对照组痊愈6例,显效10例,总有效率为53.3%。两组结果经统计学处理,χ2=4.8,差异具有显著性(P<0.05)。结论莫匹罗欣软膏联合阿达帕林凝胶是治疗寻常型痤疮的有效方法之一,值得临床推广应用。     

夫西地酸软膏联合阿达帕林凝胶治疗寻常型痤疮临床观察

目的观察夫西地酸软膏联合阿达帕林凝胶治疗寻常型痤疮的临床疗效和安全性。方法寻常型痤疮82例,随机分为2组。治疗组42例,外用夫西地酸软膏,每日1次,外用0.1%阿达帕林凝胶,每晚1次,连用8周;对照组40例,外用0.1%阿达帕林凝胶,每晚1次,连用8周。停药后观察其疗效。结果治疗组基本痊愈16例,显效14例,总有效率为71.4%;对照组痊愈7例,显效12例,总有效率为47.5%。2组结果经统计学处理,χ2=4.878,差异具有显著性(P<0.05)。结论夫西地酸软膏联合阿达帕林凝胶是治疗寻常型痤疮的有效方法之一,值得临床推广应用。     

万苏平治疗2型糖尿病84例临床疗效观察

目前国内已有多个厂家生产格列美脲,并已在临床上应用,但其临床研究资料相对较少。为了进一步观察国产格列美脲的临床疗效及安全性,自2006年2月至2008年4月,我们观察了84例以国产GM万苏平为主配合拜糖苹治疗2型糖尿病的临床疗效和安全性,现报道并分析如下。     

胰岛素泵治疗2型糖尿病的临床疗效观察

目的对比胰岛素泵持续皮下输注法(CSII)和多次胰岛素注射法(MDII)治疗2型糖尿病的临床疗效。方法将50例2型糖尿病人随机分为两组,分别为CSII治疗组,MDII治疗组。结果两种方法均能有效降低血糖,改善临床症状,但血糖达标,胰岛素总用量CSII组明显少于MDII组;所需时间,CSII组明显短于MDII组;低血糖发生率,CSII组明显低于MDII组。结论胰岛素泵持续皮下输注法治疗2型糖尿病,能更快更平稳的降低血糖,降低低血糖发生率,减少胰岛素的用量,显著地降低糖化血红蛋白,从而有效的减少糖尿病急慢性并发症的发生率,各种疗效明显优于多次胰岛素皮下注射治疗法。     

The Role of Autophagy in Lupus Nephritis

Systemic lupus erythematosus (SLE) is a multifactorial autoimmune disease characterized by the generation of immune responses to self-antigens. Lupus nephritis is one of the most common and severe complications in SLE patients. Though the pathogenesis of lupus nephritis has been studied extensively, unresolved questions are still left and new therapeutic methods are needed for disease control. Autophagy is a conserved catabolic process through which cytoplasmic constituents can be degraded in lysosome and reused. Autophagy plays vital roles in maintaining cell homeostasis and is involved in the pathogenesis of many diseases. In particular, autophagy can affect almost all parts of the immune system and is involved in autoimmune diseases. Based on genetic analysis, cell biology, and mechanism studies of the classic and innovative therapeutic drugs, there are growing lines of evidence suggesting the relationship between autophagy and lupus nephritis. In the present review, we summarize the recent publications investigating the relationship between autophagy and lupus nephritis and provide a new perspective towards the pathogenesis of lupus nephritis.     

Advances in Lupus Nephritis Pathogenesis: From Bench to Bedside

Systemic lupus erythematosus (SLE) is the prototype of autoimmune disorders caused by a loss of tolerance to endogenous nuclear antigens triggering an aberrant autoimmune response targeting various tissues. Lupus nephritis (LN), a major cause of morbidity and mortality in patients with SLE, affects up to 60% of patients. The recent insights into the genetic and molecular basis of SLE and LN paved the way for newer therapies to be developed for these patients. Apart from the traditional B-cell-centered view of this disease pathogenesis, acknowledging that multiple extrarenal and intrarenal pathways contribute to kidney-specific autoimmunity and injury may help refine the individual therapeutic and prognostic characterization of such patients. Accordingly, the formerly induction-maintenance treatment strategy was recently challenged with the exciting results obtained from the trials that evaluated add-on therapy with voclosporin, belimumab, or Obinutuzumab. The scope of this review is to provide an insight into the current knowledge of LN pathogenesis and future therapeutic strategies.     

Biomarkers for Refractory Lupus Nephritis: A Microarray Study of Kidney Tissue

The prognosis of severe lupus nephritis (LN) is very different among individual patients. None of the current biomarkers can be used to predict the development of refractory LN. Because kidney histology is the gold standard for diagnosing LN, the authors hypothesize that molecular signatures detected in kidney biopsy tissue may have predictive value in determining the therapeutic response. Sixty-seven patients with biopsy-proven severely active LN by International Society of Nephrology/Renal Pathology Society (ISN/RPS) classification III/IV were recruited. Twenty-three kidney tissue samples were used for RNA microarray analysis, while the remaining 44 samples were used for validation by real-time polymerase chain reaction (PCR) gene expression analysis. From hundreds of differential gene expressions in refractory LN, 12 candidates were selected for validation based on gene expression levels as well as relevant functions. The candidate biomarkers were members of the innate immune response molecules, adhesion molecules, calcium-binding receptors, and paracellular tight junction proteins. S100A8, ANXA13, CLDN19 and FAM46B were identified as the best kidney biomarkers for refractory LN, and COL8A1 was identified as the best marker for early loss of kidney function. These new molecular markers can be used to predict refractory LN and may eventually lead to novel molecular targets for therapy.     

Exhausted but Not Senescent T Lymphocytes Predominate in Lupus Nephritis Patients

Lupus nephritis (LN), a chronic inflammatory disease, is characterized by the substantial disruption of immune homeostasis. This study examines its effects on the T lymphocyte phenotype and, particularly, its senescence- and exhaustion-related immune alterations. T cell subpopulations were determined with flow cytometry in 30 LN patients and 20 healthy controls (HCs), according to the expression of senescence- (CD45RA, CCR7, CD31, CD28, CD57), and exhaustion- (PD1) related markers. The immune phenotype was associated with disease activity and renal histology. LN patients were characterized by pronounced lymphopenia, mainly affecting the CD4 compartment, with a concurrent reduction in the naïve, central and effector memory subsets compared to the HCs. In the CD8 compartment, the naïve subsets were significantly lower than that of the HCs, but a shift in the T cells occurred towards the central memory population. CD4+PD1+ and CD8+PD1+ cells were increased in the LN patients compared to the HCs. However, in CD4 T cells, the increase was limited to CD45RA+, whereas in CD8 T cells, both CD45RA+ and CD45RA− subsets were affected. Disease activity was correlated with CD4+PD1+ and highly differentiated CD4+CD28-CD57+ cells. Histology was only associated with CD4 T cell disturbances, with stage IV presenting reduced naïve and increased senescent subsets. Exhausted T lymphocyte subpopulations predominate within LN patients, while the T cell phenotype varies depending on disease activity.     

MicroRNAs in Lupus Nephritis–Role in Disease Pathogenesis and Clinical Applications

MicroRNAs (miRs) are non-coding small RNAs that act as epigenetic modulators to regulate the protein levels of target mRNAs without modifying the genetic sequences. The role of miRs in the pathogenesis of lupus nephritis (LN) is increasingly recognized and highly complex. Altered levels of different miRs are observed in the blood, urine and kidney tissues of murine LN models and LN patients. Accumulating evidence suggests that these miRs can modulate immune cells and various key inflammatory pathways, and their perturbations contribute to the aberrant immune response in LN. The dysregulation of miRs in different resident renal cells and urinary exosomes can also lead to abnormal renal cell proliferation, inflammation and kidney fibrosis in LN. While miRs may hold promise in various clinical applications in LN patients, there are still many potential limitations and safety concerns for their use. Further studies are worthwhile to examine the clinical utility of miRs in the diagnosis, disease activity monitoring, prognostication and treatment of LN.