成人HIV/AIDS病人HAART前血小板减少的发生率及相关因素分析

目的描述成人艾滋病病毒(HIV)感染者/艾滋病(AIDS)病人(简称HIV/AIDS病人)在高效抗病毒治疗(HAART)前,发生血小板减少的基本特征,探讨HIV合并血小板减少的发生率及相关因素。方法以2003年6月至2015年12月,在北京地坛医院门诊就诊的3452例HIV/AIDS病人为研究对象,比较HAART前不同基本情况[人口学资料、身体质量指数(BMI)、CD4+T淋巴细胞(简称CD4细胞)计数、病毒载量、是否合并机会性感染及症状体征、其他混合性感染的合并情况及是否服用复方新诺明(SMZ-TMP)情况]的血小板减少的发生率,通过Logistic回归分析HIV/AIDS病人合并血小板减少症的相关因素。结果 HAART前合并血小板减少的有137例(3.97%),其中轻度104例(3.01%),中度19例(0.55%),重度14例(0.41%)。血小板减少的发生率随CD4细胞计数的增加而降低(P0.001)。HAART前HIV RNA≥105拷贝/mL[调整OR值(AOR)=1.903,95%CI:1.125~3.218,P=0.016],CD4细胞计数≤50个/μL(AOR=8.828,95%CI:2.939~26.519,P0.001)及CD4细胞计数51~199个/μL(AOR=3.714,95%CI:1.317~10.479,P=0.013),HBsAg+(AOR=4.949,95%CI:2.372~10.323,P0.001)是发生血小板减少的危险因素。结论成人HIV/AIDS病人HAART前血小板减少发生率较低。低基线CD4细胞计数、高基线病毒载量及合并乙型肝炎是HAART前发生血小板减少的相关因素,因此对存在这些危险因素的病人及早的诊断和治疗是必须的。     

成人HIV/AIDS病人HAART前血小板减少的发生率及相关因素分析北大核心

目的描述成人艾滋病病毒（HIV）感染者/艾滋病（AIDS）病人（简称HIV/AIDS病人）在高效抗病毒治疗（HAART）前,发生血小板减少的基本特征,探讨HIV合并血小板减少的发生率及相关因素。方法以2003年6月至2015年12月,在北京地坛医院门诊就诊的3452例HIV/AIDS病人为研究对象,比较HAART前不同基本情况[人口学资料、身体质量指数（BMI）、CD4^＋T淋巴细胞（简称CD4细胞）计数、病毒载量、是否合并机会性感染及症状体征、其他混合性感染的合并情况及是否服用复方新诺明（SMZ-TMP）情况]的血小板减少的发生率,通过Logistic回归分析HIV/AIDS病人合并血小板减少症的相关因素。结果 HAART前合并血小板减少的有137例（3.97%）,其中轻度104例（3.01%）,中度19例（0.55%）,重度14例（0.41%）。血小板减少的发生率随CD4细胞计数的增加而降低（P〈0.001）。HAART前HIV RNA≥105拷贝/mL[调整OR值（AOR）=1.903,95%CI：1.125-3.218,P=0.016],CD4细胞计数≤50个/μL（AOR=8.828,95%CI：2.939-26.519,P〈0.001）及CD4细胞计数51-199个/μL（AOR=3.714,95%CI：1.317-10.479,P=0.013）,HBsAg＋（AOR=4.949,95%CI：2.372-10.323,P〈0.001）是发生血小板减少的危险因素。结论成人HIV/AIDS病人HAART前血小板减少发生率较低。低基线CD4细胞计数、高基线病毒载量及合并乙型肝炎是HAART前发生血小板减少的相关因素,因此对存在这些危险因素的病人及早的诊断和治疗是必须的。     

中药(XQ-9302)治疗HIV感染者/AIDS患者CD4细胞计数和病毒载量变化的评价

目的　探讨中药 (XQ 930 2 )对艾滋病病毒 (HIV)感染者 /艾滋病 (AIDS)患者的治疗作用。方法　测定XQ 930 2治疗 2 1例HIV感染者 /AIDS患者的CD4细胞计数和病毒载量 ,并与仅进行对症治疗的HIV感染者 /AIDS患者对照组比较。结果　经XQ 930 2治疗后 ,4 2 9%HIV感染者 /AIDS患者的CD4细胞计数上升 >5 1% ,为显效 ;33 3%患者的CD4细胞计数升高 11%～ 5 0 % ,为有效 ,总有效率为 76 2 % ;CD4细胞计数上升 <10 %为无效 ,无效率为 2 3 8%。 5 2 4 %HIV感染者 /AIDS患者的病毒载量下降≥ 1log ,呈显效 ;38 1%的HIV感染者 /AIDS患者病毒载量无变化或下降 <1log ,为有效 ;仅 9 5 %HIV感染者 /AIDS患者病毒载量上升 ,为无效。所有HIV感染者 /AIDS患者的临床症状均获改善。对照组HIV感染者 /AIDS患者病毒载量呈稳定及上升状态 ,临床症状均未获改善 ,呈无效。结论　XQ 930 2对HIV感染者 /AIDS患者的CD4细胞计数上升以及病毒载量下降有效 ,且能改善临床症状。     

HIV／AIDS患者血浆病毒载量及外周血T淋巴细胞亚群的变化

目的：观察国内HIV／AIDS患者血浆病毒载量和外周血CD4^ 、CD8^ T淋巴细胞的变化，探讨这些变化的临床意义。方法：选择未经抗病毒治疗的HIV／AIDS患者124例，用bDNA法检测血浆病毒载量，并用流式细胞仪检测外周血CD4^ 、CD8^ T淋巴细胞。结果：AIDS患者的血浆病毒载量明显高于HIV感染者，血浆病毒载量与CD4^ 细胞计数呈显著负相关，但其最高峰位于CD4^ 细胞计数100／μl处，然后随着CD4^ 细胞计数的下降而减少。CD4^ T细胞计数为AIDS组＜HIV组＜正常对照组：HIV感染者的CD8^ T细胞计数显著高于正常组和AIDS组，而AIDS患者CD8^ T细胞数则随着CD4^ T细胞减少而下降。结论：血浆病毒载量随着疾病进展而显著升高，但在疾病晚期则有所降低。外周血CD4^ T细胞计数随着疾病的进展而进行性减少；CD8^ T细胞计数在感染早期显著升高，进入晚期则减少。在评价HIV感染者和AIDS患者病情时，应结合病毒载量、CD4^ 、CD8^ T细胞计数综合分析。     

人类免疫缺陷病毒合并结核分枝杆菌感染者的抗结核细胞免疫功能

目的 评价HIV合并结核分枝杆菌潜伏感染或合并活动性结核患者的抗结核细胞免疫功能.方法 应用早期分泌性抗原靶蛋白(ESAT)-6和培养滤出蛋白(CFP)-10诱导的结核酶联免疫斑点法对云南地区100例明确诊断的HIV感染者的血液标本进行结核分枝杆菌特异性T淋巴细胞检测,同时应用流式细胞仪检测外周血CD3+CD4+T淋巴细胞和CD3+CD8+T淋巴细胞的绝对计数水平.采用Mann-Whitney检验进行非参数统计分析.结果临床上无活动性结核感染证据的HIV感染者中合并结核分枝杆菌潜伏感染的感染率高达67.6%.HIV合并结核分枝杆菌潜伏感染者的外周血CD3+CD4+T淋巴细胞(532×106/L)和CD3+CD8+T淋巴细胞(473×106/L)绝对计数与单纯HIV感染者(406×106/L和504 × 106/L)相比,差异无统计学意义.HIV合并活动性结核感染者的外周血CD3+CD4+T淋巴细胞绝对计数平均值为189 × 106/L,CD3+CD8+T淋巴细胞绝对计数平均值为293×106/L,均显著低于单纯HIV合并结核潜伏感染组和HIV组(U=168.0,U=163.0;U=147.0,U=374.0;均P<0.01).HIV合并活动性结核感染者的ESAT-6和CFP-10抗原特异性斑点形成细胞数(31/106细胞和82/106细胞)显著低于HIV合并结核分枝杆菌潜伏感染者(92/106细胞和109/106细胞.U=507.0,U=529.5,均P<0.01).结论 我国无活动性结核临床证据的HIV感染人群中有较高的结核潜伏感染率,HIV合并活动性结核感染者的总体细胞免疫应答功能及特异性抗结核免疫应答功能均严重受损.     

HIV感染者/AIDS患者与肿瘤病人T淋巴细胞亚群数量的比较

目的　探讨艾滋病病毒 (HIV)感染者和艾滋病 (AIDS)患者与肿瘤病人CD+4和CD+8T淋巴细胞 (TH 和TS 细胞 )数量的变化并进行比较。方法　用流式细胞仪检测 78例HIV感染者 /AIDS患者和 37例肿瘤病人外周血中TH 和TS 细胞的数量以及计算TH/TS 的比值 ,组间比较采用双侧t检验。结果　HIV感染者 /AIDS患者TH细胞显著减少 ,且下降的幅度大 ,TH<5 0 0 / μl的占 83 3% ,其中 <2 0 0 / μl的占 5 6 4 % ,TH/TS 平均为 0 2 9;肿瘤病人TH 细胞计数也明显降低 ,TH<5 0 0 / μl的占 70 3% ,其中 <2 0 0 / μl的占 18 9% ,TH/TS 平均为 1 2 6。同一水平CD+4T细胞计数所对应的CD+8T细胞数量 ,HIV感染者 /AIDS患者高于肿瘤病人 ;两组病人TS 数量都随TH 数量的升高而增加。HIV感染者 /AIDS患者TH 细胞计数 <肿瘤病人 ,TS 细胞计数 >肿瘤病人 ,HIV感染者 /AIDS患者TH/TS 比值倒置 ,而肿瘤病人TH/TS 比值 >1。结论　HIV感染者 /AIDS患者和肿瘤病人存在不同程度的细胞免疫功能损害 ,T淋巴细胞亚群的检测可作为两者免疫诊断和免疫功能监测的指标之一 ,对于病人的治疗和预后有一定的意义     

广东省某市871例HIV/AIDS病人生存影响因素的回顾性队列研究

目的利用艾滋病综合防治信息系统了解艾滋病病毒（HIV）感染者/艾滋病（AIDS）病人（简称HIV/AIDS病人）生存的影响因素。方法采用回顾性队列研究方法,了解HIV/AIDS病人被确证感染后的转归及相关情况。结果 HIV/AIDS病人被确证时的年龄是影响生存时间的重要因素[风险值（HR）=1.04,95%可信区间（CI）：1.01-1.06,P〈0.01]。是否接受抗病毒治疗（HR=0.10,95%CI：0.03-0.33,P〈0.01）及初次CD^＋_4T淋巴细胞计数分级则是影响HIV/AIDS病人生存的保护性因素（HR=0.69,95%CI：0.58-0.82,P〈0.01）,接受抗病毒治疗、初次CD＋4T淋巴细胞计数分级高的生存时间长,差异具有统计学意义。结论早发现、早治疗有利于提高HIV/AIDS病人的生存时间。     

HIV合并HCV感染患者的血液相关检测分析

目的分析艾滋病病毒(HIV)/丙型肝炎病毒(HCV)合并感染人群抗病毒治疗前血液相关检测结果特征及其对临床治疗的指导价值。方法回顾性分析广州市第八人民医院2009—2016年间收治的HIV感染者/AIDS病人(简称HIV/AIDS病人)、HIV/HCV合并感染者和HCV感染者抗病毒治疗前的实验室检测资料,对收集的病人免疫细胞计数和血常规相关检测指标,采用秩和检验进行统计分析,统计软件为SPSS 19.0。结果共入组196例病人,其中HIV单一感染者75例,HIV/HCV合并感染者76例,HCV单一感染组45例。分析HIV单一感染组和HIV/HCV合并感染组之间CD4+T淋巴细胞(简称CD4细胞)计数及CD8+T淋巴细胞(简称CD8细胞)计数、CD4/CD8比值,结果显示:HIV/HCV合并感染组的CD4细胞、CD8细胞计数和CD4/CD8比值较HIV单一感染组无显著差异(Z=-1.319,P=0.187;Z=-0.171,P=0.864;Z=-1.560,P=0.119);三组间血常规各项指标检测结果显示:HIV/HCV合并感染组红细胞(RBC)、血红蛋白(HGB)、平均红细胞体积、平均红细胞血红蛋白含量(MCH)、平均红细胞血红蛋白浓度、RBC差值、HGB差值与HIV单一感染组及HCV单一感染组比较差异均有统计学意义(P均0.05),HIV单一感染组与HCV单一感染组间差异无统计学意义(P0.05)(除MCH外)。结论排除肝功能异常的影响后,合并HCV感染未显著影响HIV/AIDS病人外周血免疫细胞计数,但合并HCV感染的HIV/AIDS病人抗病毒治疗前更易发生贫血,且以小细胞低色素性贫血类型为主,提示HIV/HCV合并感染者的临床治疗需要更多关注贫血发生。     

乌鲁木齐市天山区75例HIV/AIDS患者流行病学分析

目的 分析乌鲁木齐市天山区HIV/AIDS患者的流行病学特点.方法分析2008年乌鲁木齐市天山区艾滋病综合防治示范区75 例HIV/AIDS患者的流行病学特点、CD4 T细胞水平及HIV 相关机会性感染特点.结果 HIV感染者中维吾尔族占88%,汉族5%,回族7%;HIV 感染平均年龄为(34±6.74)岁;男性占73%,女性占27%;感染途径主要是静脉吸毒(83%) 及性传播(17%);合并HCV感染者占 87%;HIV 感染者中大部分为无业人员(52%);机会性感染以结核病为主(24%);CD4 细胞计数<300 个/μL 的HIV 感染者占35 %.结论乌鲁木齐市天山区综合防治示范区收治的HIV/AIDS患者的主要特点是年轻发病多见,维吾尔族患者较多;大多数患者因静脉吸毒而感染并合并感染HCV,结核是最为常见的机会性感染.     

HIV/AIDS患者死亡危险因素Logistic回归分析

目的 探讨HIV/AIDS患者死亡相关危险因素,为降低HIV/AIDS病死率提供参考.方法 选取HIV/AIDS患者11482例,其中死亡500例,采用Logistic回归分析法分析死亡相关危险因素.结果 患者性别、年龄、文化程度、感染途径、CD4+T淋巴细胞计数与死亡的发生有显著相关性.结论 男性、年龄大、文化程度低、感染途径为有偿供血和吸毒、CD4+T淋巴细胞计数低,是HIV/AIDS患者预后不良的危险因素.临床上对有上述危险因素的HIV/AIDS患者,应加强医疗和社会支持,提高其生活质量,以降低病死率.     

Living Donor Kidney Transplantation: Improving Efficiencies in Live Kidney Donor Evaluation–Recommendations from a Consensus Conference

The education, evaluation, and support of living donors before, during, and after donation have historically been considered the roles and responsibilities of transplant programs. Although intended to protect donors, ensure true informed consent, and prevent coercion, this structure often leaves referring nephrologists unclear about the donor process and uncertain regarding the ultimate outcome of potential donors for their patients. The aim of this article is to help the referring nephrologist understand the donor referral and evaluation process, help the referring nephrologist understand the responsibilities of the transplant program, and offer suggestions about how the referring nephrologist can help to improve efficiencies in the process of donor education and evaluation. A partnership between referring nephrologists and transplant programs is an important step in advancing living kidney donation. The referring nephrologists are the frontline providers and are in a unique position to offer education about living donation and improve efficiencies in the process. Understanding the donor referral and evaluation process, the responsibilities of the transplant program, and the potential role referring nephrologists can play in the process is critical to establishing such a partnership.     

系膜IgA沉积的供肾移植后的转归

目的 :探讨接受系膜IgA沉积的供肾移植后的临床转归。　 方法 :对供肾进行常规活检 ,比较系膜IgA沉积供肾 (IgA供肾组 ,n =83)与系膜无IgA沉积供肾 (无IgA供肾组 ,n =2 5 9)移植后的转归 ,以及两组之间性别、年龄、透析时间、供肾冷热缺血时间、补体依赖性微量淋巴细胞毒、群体反应性抗体水平和原发病的分布。　 结果 :2 4 3%的受者接受了IgA沉积的供肾。IgA沉积供肾组术后浮肿、蛋白尿、血尿、低白蛋白血症、高血压和移植肾功能延迟恢复的发生率明显高于无IgA供肾组。肾移植 3个月内 ,IgA沉积供肾组急性排斥反应发生率明显高于无IgA沉积供肾组 ,分别为 31 3%和 19 3%(P <0 0 0 1)。临界改变发生率分别为 37 3%和 16 2 %(P <0 0 0 1)。随着移植时间推移 ,IgA沉积供肾组IgA沉积例数逐渐减少 ,术后 1、3和 6个月仍有系膜IgA沉积者分别为 2 6例(31 3%)、9例 (10 8%)和 2例 (2 4 %) ,至 6个月时与对照组比较差异不明显。两组间 1年肾存活率差异不显著 ,分别为 93 8%和 95 6 %,3年存活率分别为 86 7%和 88 3%。　 结论 :系膜IgA沉积的供肾移植后移植肾功能延迟恢复和急性排斥反应的发生率明显高于无IgA沉积供肾组 ,但不影响远期肾存活率 ,且系膜区IgA沉积可以逐渐消失。     

Clinical and Genetic Analysis of Patients with Cystinuria in the United Kingdom

Background and objectives

Cystinuria is a rare inherited renal stone disease. Mutations in the amino acid exchanger System b^0,+, the two subunits of which are encoded by SLC3A1 and SLC7A9, predominantly underlie this disease. The work analyzed the epidemiology of cystinuria and the influence of mutations in these two genes on disease severity in a United Kingdom cohort.

Design, setting, participants, & measurements

Prevalent patients were studied from 2012 to 2014 in the northeast and southwest of the United Kingdom. Clinical phenotypes were defined, and genetic analysis of SLC3A1 and SLC7A9 combining Sanger sequencing and multiplex ligation probe–dependent amplification was performed.

Results

In total, 76 patients (42 men and 34 women) were studied. All subjects had proven cystine stones. Median age of presentation (first stone episode) was 24 years old, but 21% of patients presented after 40 years old. Patients had varied clinical courses, with 37% of patients having ≥10 stone episodes; 70% had evidence of CKD, and 9% had reached ESRD as a result of cystinuria and its complications. Patients with cystinuria received a variety of different therapies, with no obvious treatment consensus. Notably, 20% of patients had staghorn calculi, with associated impaired renal function in 80% of these patients. Genetic analysis revealed that biallelic mutations were present in either SLC3A1 (n=27) or SLC7A9 (n=20); 22 patients had only one mutated allele detected (SLC3A1 in five patients and SLC7A9 in 17 patients). In total, 37 different mutant variant alleles were identified, including 12 novel mutations; 22% of mutations were caused by large gene rearrangements. No genotype-phenotype association was detected in this cohort.

Conclusions

Patients with cystinuria in the United Kingdom often present atypically with staghorn calculi at ≥40 years old and commonly develop significant renal impairment. There is no association of clinical course with genotype. Treatments directed toward reducing stone burden need to be rationalized and developed to optimize patient care.     

Forced expression of laminin beta1 in podocytes prevents nephrotic syndrome in mice lacking laminin beta2, a model for Pierson syndrome

Pierson syndrome is a congenital nephrotic syndrome with ocular and neurological defects caused by mutations in LAMB2, the gene encoding the basement membrane protein laminin β2 (Lamβ2). It is the kidney glomerular basement membrane (GBM) that is defective in Pierson syndrome, as Lamβ2 is a component of laminin-521 (LM-521; α5β2γ1), the major laminin in the mature GBM. In both Pierson syndrome and the Lamb2(-/-) mouse model for this disease, laminin β1 (Lamβ1), a structurally similar homolog of Lamβ2, is marginally increased in the GBM, but it fails to fully compensate for the loss of Lamβ2, leading to the filtration barrier defects and nephrotic syndrome. Here we generated several lines of Lamβ1 transgenic mice and used them to show that podocyte-specific Lamβ1 expression in Lamb2(-/-) mice abrogates the development of nephrotic syndrome, correlating with a greatly extended lifespan. In addition, the more Lamβ1 was expressed, the less urinary albumin was excreted. Transgenic Lamβ1 expression increased the level of Lamα5 in the GBM of rescued mice, consistent with the desired increased deposition of laminin-511 (α5β1γ1) trimers. Ultrastructural analysis revealed occasional knob-like subepithelial GBM thickening but intact podocyte foot processes in aged rescued mice. These results suggest the possibility that up-regulation of LAMB1 in podocytes, should it become achievable, would likely lessen the severity of nephrotic syndrome in patients carrying LAMB2 mutations.     

Different Aspects of Kidney Function in Well-Controlled Congenital Hypothyroidism

Objective: Congenital hypothyroidism (CH) increases the prevalence of kidney and urogenital malformations. There are limited studies considering different aspects of kidney function in well-controlled CH patients. We evaluated some features of kidney function in euthyroid children with CH who have been receiving thyroxine hormone since early life.Methods: This cross-sectional study was conducted in Isfahan, Iran, on 74 children aged 2-15 years old (36 CH patients and 38 healthy children). Inclusion criteria for CH patients were euthyroidism at the time of the survey and initiation of replacement therapy during the early neonatal period. Kidney ultrasound evaluation was performed in all participants. Serum biochemistry included urea, creatinine, sodium (Na), potassium (K), magnesium, calcium, and cystatin C levels. Urine electrolytes, fraction excretion (FE) of electrolytes and microalbumin, and glomerular filtration rate (GFR) were also determined.Results: The male/female ratio was 0.8/1 and 1.5/1 in the patient and control groups, respectively. Mean age and height did not differ significantly between the two groups. Ultrasound evaluation of the kidney revealed that the anteroposterior diameter of the right kidney was significantly higher in CH patients as compared to healthy subjects. No significant difference was observed between GFRs in patients with CH and healthy children. The mean values for FENa and FEK were significantly higher in the patient group.Conclusions: Increased FENa and FEK may be a manifestation of impaired tubular maturation in CH. More longitudinal studies are needed to evaluate kidney function in CH patients. Conflict of interest:None declared.     

20665例普通人群单次尿液和肾功能检查结果及其意义探讨

目的:了解普通人群健康体检时尿检异常(蛋白尿、血尿、白细胞尿)和肾功能减退的检出率,探讨其临床意义。方法:筛查2008-08-12复旦大学附属中山医院健康体检人群的尿液和肾功能检查资料。肾功能减退标准为血清肌酐mg/dl(μmol/L):(1)KEEP标准男性1.5(133),女性1.3(115);(2)NHANES Ⅲ标准男性1.4(124),女性1.2(106),老年(≥65岁)男性≥1.3(115),女性≥1.0(88.4)。结果:共20 665例,其中男性13 320例(64.46%),女性7 345例(35.54%)。尿检异常检出率5.27%,其中男性3.64%,女性8.22%(P0.01);蛋白尿2.68%,男性2.72%,女性2.60%,P0.01;血尿2.41%,男性1.47%,女性4.11%,P0.01;白细胞尿1.71%,男性0.46%,女性4.00%,P0.01。按照KEEP和NHANES Ⅲ标准,肾功能减退检出率分别为0.26%和0.76%,男性和女性分别为0.20%和0.38%(P0.05),0.35%和0.98%(P0.01)。尿检异常人群肾功能减退的检出率显著高于尿检正常人群(KEEP标准1.3%和0.2%,P0.01;NHANES Ⅲ标准2.0%和0.5%,P0.01);肾功能减退人群尿检异常的检出率显著高于肾功能正常人群(KEEP标准25.9%和5.2%,P0.01;NHANES Ⅲ标准18.6%和5.2%,P0.01)。结论:普通人群尿检异常和肾功能减退检出率较高。在健康体检中应重视尿液和肾功能检查,以提高肾脏病的检出率。     

Platelet counts in autosomal dominant polycystic kidney disease

Platelet counts in patients with autosomal dominant polycystic kidney disease (ADPKD) have been reported to be lower than in control populations in one small study but data are sparse. We retrospectively audited real world platelet data from 290 ADPKD patients with corresponding age and sex-matched controls. We analysed 42?972 individual blood counts and patients with ADPKD had statistically lower platelet counts (213?±?63 vs. 238?±?69?×?10⁹/L, p?相似文献